Bioactive Compounds and Therapeutics: Molecular Aspects, Metabolic Profiles, and Omics Studies

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Biomolecules biomolecules	4.8	9.4	2011	16.3 Days	CHF 2700
Cells cells	5.1	9.9	2012	17.5 Days	CHF 2700
International Journal of Molecular Sciences ijms	4.9	8.1	2000	18.1 Days	CHF 2900
Metabolites metabolites	3.4	5.7	2011	13.9 Days	CHF 2700
Molecules molecules	4.2	7.4	1996	15.1 Days	CHF 2700

12 pages, 3575 KiB

Open AccessArticle

NBF2, an Algal Fiber-Rich Formula, Reverses Diabetic Dyslipidemia and Hyperglycemia In Vivo

by Nlandu Roger Ngatu, Akram Hossain, Nao Maruo, Steeve Akumwami, Asadur Md. Rahman, Masamitsu Eitoku, Kanae Kanda, Akira Nishiyama, Narufumi Suganuma and Tomohiro Hirao

Int. J. Mol. Sci. 2024, 25(19), 10828; https://doi.org/10.3390/ijms251910828 - 9 Oct 2024

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Abstract

Ulva prolifera, known as Aonori in Japan, is an edible alga species that is mass-cultivated in Japan. Supplementation with Aonori-derived biomaterials has been reported to enhance metabolic health in previous studies. This was an experimental study that evaluated the metabolic health effects [...] Read more.

Ulva prolifera, known as Aonori in Japan, is an edible alga species that is mass-cultivated in Japan. Supplementation with Aonori-derived biomaterials has been reported to enhance metabolic health in previous studies. This was an experimental study that evaluated the metabolic health effects of NBF2, a formula made of algal and junos Tanaka citrus-derived biomaterials, on obesity and type 2 diabetes (T2DM). We used 18 obese and hyperglycemic Otsuka Long-Evans Tokushima Fatty (OLETF) rats that were assigned randomly to three groups of six animals: a high-dose NBF2 drink (20 mg/kg) group, a low-dose (10 mg/kg) NBF2 drink group and the control group that received 2 mL of tap water daily for a total of six weeks. We also used eight LETO rats as the normal control group. In addition to the glucose tolerance test (OGTT), ELISA and real-time PCR assays were performed. High-dose and lowdose NBF2 improved insulin sensitivity, as well as glycemic and lipid profiles, as compared with control rats. The OGTT showed that both NBF2 groups and LETO rats had normalized glycemia by the 90-min time-point. NBF2 up-regulated PPARα/γ-mRNA and Sirt2-mRNA gene expressions in BAT and improved the blood pressure profile. These findings suggest that the NBF2 formula, which activates PPAR-α/γ mRNA and Sirt2-mRNA, may reverse dyslipidemia and hyperglycemia in T2DM. Full article

(This article belongs to the Topic Bioactive Compounds and Therapeutics: Molecular Aspects, Metabolic Profiles, and Omics Studies)

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17 pages, 6986 KiB

Open AccessArticle

Ursolic Acid Regulates Immune Balance, Modulates Gut Microbial Metabolism, and Improves Liver Health in Mice

by Man Zhao, Yali Cui, Fengxia Wang, Fengyang Wu, Chong Li, Shudong Liu and Baojiang Chen

Int. J. Mol. Sci. 2024, 25(19), 10623; https://doi.org/10.3390/ijms251910623 - 2 Oct 2024

Viewed by 543

Abstract

Ursolic acid (UA) has demonstrated significant immunomodulatory and hepatoprotective effects; however, the underlying mechanisms remain unclear. This study aims to analyze the impact of UA on the gut microbiome, metabolome, and liver transcriptome, investigate UA’s role in maintaining gut immune homeostasis and liver [...] Read more.

Ursolic acid (UA) has demonstrated significant immunomodulatory and hepatoprotective effects; however, the underlying mechanisms remain unclear. This study aims to analyze the impact of UA on the gut microbiome, metabolome, and liver transcriptome, investigate UA’s role in maintaining gut immune homeostasis and liver health, and evaluate the potential contributions of gut microbes and their metabolites to these beneficial effects. Our findings indicate that UA enhances immune balance in the jejunum, fortifies intestinal barrier function, and promotes overall gut health. UA modulates the intestinal microbiota and its metabolic processes, notably increasing the abundance of beneficial bacteria such as Odoribacter and Parabacteroides, along with their metabolites, including ornithine and lactucin. Additionally, UA inhibits the expression of interleukin-1 receptor 1 (IL1R1) and calcium (Ca²⁺) voltage-gated channel auxiliary subunit beta 2 (CACNB2) while enhancing the synthesis pathways of retinol and ascorbic acid, thereby exerting a protective influence on liver function. In summary, UA enhances intestinal immune homeostasis and promotes liver health, with these advantageous effects potentially mediated by beneficial bacteria (Odoribacter and Parabacteroides) and their metabolites (ornithine and lactucin). Full article

(This article belongs to the Topic Bioactive Compounds and Therapeutics: Molecular Aspects, Metabolic Profiles, and Omics Studies)

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17 pages, 4135 KiB

Open AccessArticle

GPR40/GPR120 Agonist GW9508 Improves Metabolic Syndrome-Exacerbated Periodontitis in Mice

by Yanchun Li, Hong Yu, Maria F. Lopes-Virella and Yan Huang

Int. J. Mol. Sci. 2024, 25(17), 9622; https://doi.org/10.3390/ijms25179622 - 5 Sep 2024

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Abstract

G protein-coupled receptor (GPR)40 and GPR120 are receptors for medium- and long-chain free fatty acids. It has been well documented that GPR40 and GPR120 activation improves metabolic syndrome (MetS) and exerts anti-inflammatory effects. Since chronic periodontitis is a common oral inflammatory disease initiated [...] Read more.

G protein-coupled receptor (GPR)40 and GPR120 are receptors for medium- and long-chain free fatty acids. It has been well documented that GPR40 and GPR120 activation improves metabolic syndrome (MetS) and exerts anti-inflammatory effects. Since chronic periodontitis is a common oral inflammatory disease initiated by periodontal pathogens and exacerbated by MetS, we determined if GPR40 and GPR120 activation with agonists improves MetS-associated periodontitis in animal models in this study. We induced MetS and periodontitis by high-fat diet feeding and periodontal injection of lipopolysaccharide, respectively, and treated mice with GW9508, a synthetic GPR40 and GPR120 dual agonist. We determined alveolar bone loss, osteoclast formation, and periodontal inflammation using micro-computed tomography, osteoclast staining, and histology. To understand the underlying mechanisms, we further performed studies to determine the effects of GW9508 on osteoclastogenesis and proinflammatory gene expression in vitro. Results showed that GW9508 improved metabolic parameters, including glucose, lipids, and insulin resistance. Results also showed that GW9508 improves periodontitis by reducing alveolar bone loss, osteoclastogenesis, and periodontal inflammation. Finally, in vitro studies showed that GW9508 inhibited osteoclast formation and proinflammatory gene secretion from macrophages. In conclusion, this study demonstrated for the first time that GPR40/GPR120 agonist GW9508 reduced alveolar bone loss and alleviated periodontal inflammation in mice with MetS-exacerbated periodontitis, suggesting that activating GPR40/GPR120 with agonist GW9508 is a potential anti-inflammatory approach for the treatment of MetS-associated periodontitis. Full article

(This article belongs to the Topic Bioactive Compounds and Therapeutics: Molecular Aspects, Metabolic Profiles, and Omics Studies)

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20 pages, 2502 KiB

Open AccessArticle

Broad-Spectrum Legionaminic Acid-Specific Antibodies in Pooled Human IgGs Revealed by Glycan Microarrays with Chemoenzymatically Synthesized Nonulosonosides

by Anoopjit Singh Kooner, Hai Yu, Shani Leviatan Ben-Arye, Vered Padler-Karavani and Xi Chen

Molecules 2024, 29(16), 3980; https://doi.org/10.3390/molecules29163980 - 22 Aug 2024

Viewed by 796

Abstract

The presence and the level of antibodies in human sera against bacterial glycans are indications of prior encounters with similar antigens and/or the bacteria that express them by the immune system. An increasing number of pathogenic bacteria that cause human diseases have been [...] Read more.

The presence and the level of antibodies in human sera against bacterial glycans are indications of prior encounters with similar antigens and/or the bacteria that express them by the immune system. An increasing number of pathogenic bacteria that cause human diseases have been shown to express polysaccharides containing a bacterial nonulosonic acid called 5,7-di-N-acetyllegionaminic acid (Leg5,7Ac₂). To investigate the immune recognition of Leg5,7Ac₂, which is critical for the fight against bacterial infections, a highly effective chemoenzymatic synthon strategy was applied to construct a library of α2–3/6-linked Leg5,7Ac₂-glycans via their diazido-derivatives (Leg5,7diN₃-glycans) formed by efficient one-pot three-enzyme (OP3E) synthetic systems from a diazido-derivative of a six-carbon monosaccharide precursor. Glycan microarray studies using this synthetic library of a Leg5,7Ac₂-capped collection of diverse underlying glycan carriers and their matched sialoside counterparts revealed specific recognition of Leg5,7Ac₂ by human IgG antibodies pooled from thousands of healthy donors (IVIG), suggesting prior human encounters with Leg5,7Ac₂-expressing pathogenic bacteria at the population level. These biologically relevant Leg5,7Ac₂-glycans and their immune recognition assays are important tools to begin elucidating their biological roles, particularly in the context of infection and host–pathogen interactions. Full article

(This article belongs to the Topic Bioactive Compounds and Therapeutics: Molecular Aspects, Metabolic Profiles, and Omics Studies)

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16 pages, 5071 KiB

Open AccessArticle

The Autophagic Activator GHF-201 Can Alleviate Pathology in a Mouse Model and in Patient Fibroblasts of Type III Glycogenosis

by Kumudesh Mishra, Sahar Sweetat, Saja Baraghithy, Uri Sprecher, Monzer Marisat, Sultan Bastu, Hava Glickstein, Joseph Tam, Hanna Rosenmann, Miguel Weil, Edoardo Malfatti and Or Kakhlon

Biomolecules 2024, 14(8), 893; https://doi.org/10.3390/biom14080893 - 24 Jul 2024

Cited by 1 | Viewed by 950

Abstract

Glycogen storage disease type III (GSDIII) is a hereditary glycogenosis caused by deficiency of the glycogen debranching enzyme (GDE), an enzyme, encoded by Agl, enabling glycogen degradation by catalyzing alpha-1,4-oligosaccharide side chain transfer and alpha-1,6-glucose cleavage. GDE deficiency causes accumulation of phosphorylase-limited [...] Read more.

Glycogen storage disease type III (GSDIII) is a hereditary glycogenosis caused by deficiency of the glycogen debranching enzyme (GDE), an enzyme, encoded by Agl, enabling glycogen degradation by catalyzing alpha-1,4-oligosaccharide side chain transfer and alpha-1,6-glucose cleavage. GDE deficiency causes accumulation of phosphorylase-limited dextrin, leading to liver disorder followed by fatal myopathy. Here, we tested the capacity of the new autophagosomal activator GHF-201 to alleviate disease burden by clearing pathogenic glycogen surcharge in the GSDIII mouse model Agl^−/−. We used open field, grip strength, and rotarod tests for evaluating GHF-201’s effects on locomotion, a biochemistry panel to quantify hematological biomarkers, indirect calorimetry to quantify in vivo metabolism, transmission electron microscopy to quantify glycogen in muscle, and fibroblast image analysis to determine cellular features affected by GHF-201. GHF-201 was able to improve all locomotion parameters and partially reversed hypoglycemia, hyperlipidemia and liver and muscle malfunction in Agl^−/− mice. Treated mice burnt carbohydrates more efficiently and showed significant improvement of aberrant ultrastructural muscle features. In GSDIII patient fibroblasts, GHF-201 restored mitochondrial membrane polarization and corrected lysosomal swelling. In conclusion, GHF-201 is a viable candidate for treating GSDIII as it recovered a wide range of its pathologies in vivo, in vitro, and ex vivo. Full article

(This article belongs to the Topic Bioactive Compounds and Therapeutics: Molecular Aspects, Metabolic Profiles, and Omics Studies)

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29 pages, 2459 KiB

Open AccessReview

Systematic Insights into the Relationship between the Microbiota–Gut–Brain Axis and Stroke with the Focus on Tryptophan Metabolism

by Xinyu Shen and Xiaoqin Mu

Metabolites 2024, 14(8), 399; https://doi.org/10.3390/metabo14080399 - 24 Jul 2024

Viewed by 1400

Abstract

Stroke, as a serious cerebral vascular disease with high incidence and high rates of disability and mortality, has limited therapeutic options due to the narrow time window. Compelling evidence has highlighted the significance of the gut microbiota and gut–brain axis as critical regulatory [...] Read more.

Stroke, as a serious cerebral vascular disease with high incidence and high rates of disability and mortality, has limited therapeutic options due to the narrow time window. Compelling evidence has highlighted the significance of the gut microbiota and gut–brain axis as critical regulatory factors affecting stroke. Along the microbiota–gut–brain axis, tryptophan metabolism further acquires increasing attention for its intimate association with central nervous system diseases. For the purpose of exploring the potential role of tryptophan metabolism in stroke and providing systematic insights into the intricate connection of the microbiota–gut–brain axis with the pathological procedure of stroke, this review first summarized the practical relationship between microbiota and stroke by compiling the latest case-control research. Then, the microbiota–gut–brain axis, as well as its interaction with stroke, were comprehensively elucidated on the basis of the basic anatomical structure and physiological function. Based on the crosstalk of microbiota–gut–brain, we further focused on the tryptophan metabolism from the three major metabolic pathways, namely, the kynurenine pathway, serotonin pathway, and microbial pathway, within the axis. Moreover, the effects of tryptophan metabolism on stroke were appreciated and elaborated here, which is scarcely found in other reviews. Hopefully, the systematic illustration of the mechanisms and pathways along the microbiota–gut–brain axis will inspire more translational research from metabolic perspectives, along with more attention paid to tryptophan metabolism as a promising pharmaceutical target in order to reduce the risk of stroke, mitigate the stroke progression, and ameliorate the stroke prognosis. Full article

(This article belongs to the Topic Bioactive Compounds and Therapeutics: Molecular Aspects, Metabolic Profiles, and Omics Studies)

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18 pages, 8312 KiB

Open AccessArticle

The Rhododendron Chrysanthum Pall.s’ Acetylation Modification of Rubisco Enzymes Controls Carbon Cycling to Withstand UV−B Stress

by Meiqi Liu, Fushuai Gong, Wang Yu, Kun Cao, Hongwei Xu and Xiaofu Zhou

Biomolecules 2024, 14(6), 732; https://doi.org/10.3390/biom14060732 - 20 Jun 2024

Viewed by 760

Abstract

Lysine acetylation of proteins plays a critical regulatory function in plants. A few advances have been made in the study of plant acetylproteome. However, until now, there have been few data on Rhododendron chrysanthum Pall. (R. chrysanthum). We analyzed the molecular [...] Read more.

Lysine acetylation of proteins plays a critical regulatory function in plants. A few advances have been made in the study of plant acetylproteome. However, until now, there have been few data on Rhododendron chrysanthum Pall. (R. chrysanthum). We analyzed the molecular mechanisms of photosynthesis and stress resistance in R. chrysanthum under UV−B stress. We measured chlorophyll fluorescence parameters of R. chrysanthum under UV−B stress and performed a multi−omics analysis. Based on the determination of chlorophyll fluorescence parameters, R. chrysanthum Y(NO) (Quantum yield of non−photochemical quenching) increased under UV−B stress, indicating that the plant was damaged and photosynthesis decreased. In the analysis of acetylated proteomics data, acetylated proteins were found to be involved in a variety of biological processes. Notably, acetylated proteins were significantly enriched in the pathways of photosynthesis and carbon fixation, suggesting that lysine acetylation modifications have an important role in these activities. Our findings suggest that R. chrysanthum has decreased photosynthesis and impaired photosystems under UV−B stress, but NPQ shows that plants are resistant to UV−B. Acetylation proteomics revealed that up- or down-regulation of acetylation modification levels alters protein expression. Acetylation modification of key enzymes of the Calvin cycle (Rubisco, GAPDH) regulates protein expression, making Rubisco and GAPDH proteins expressed as significantly different proteins, which in turn affects the carbon fixation capacity of R. chrysanthum. Thus, Rubisco and GAPDH are significantly differentially expressed after acetylation modification, which affects the carbon fixation capacity and thus makes the plant resistant to UV−B stress. Lysine acetylation modification affects biological processes by regulating the expression of key enzymes in photosynthesis and carbon fixation, making plants resistant to UV−B stress. Full article

(This article belongs to the Topic Bioactive Compounds and Therapeutics: Molecular Aspects, Metabolic Profiles, and Omics Studies)

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14 pages, 4518 KiB

Open AccessArticle

Halogenated Boroxine K₂[B₃O₃F₄OH] Modulates Metabolic Phenotype and Autophagy in Human Bladder Carcinoma 5637 Cell Line

by Nikolina Elez-Burnjaković, Lejla Pojskić, Anja Haverić, Naida Lojo-Kadrić, Maida Hadžić Omanović, Ajla Smajlović, Svetoslav Kalaydjiev, Milka Maksimović, Bojan Joksimović and Sanin Haverić

Molecules 2024, 29(12), 2919; https://doi.org/10.3390/molecules29122919 - 19 Jun 2024

Viewed by 888

Abstract

Halogenated boroxine K₂[B₃O₃F₄OH] (HB), an inorganic derivative of cyclic anhydride of boronic acid, is patented as a boron-containing compound with potential for the treatment of both benign and malignant skin changes. HB has effectively inhibited [...] Read more.

Halogenated boroxine K₂[B₃O₃F₄OH] (HB), an inorganic derivative of cyclic anhydride of boronic acid, is patented as a boron-containing compound with potential for the treatment of both benign and malignant skin changes. HB has effectively inhibited the growth of several carcinoma cell lines. Because of the growing interest in autophagy induction as a therapeutic approach in bladder carcinoma (BC), we aimed to assess the effects of HB on metabolic phenotype and autophagy levels in 5637 human bladder carcinoma cells (BC). Cytotoxicity was evaluated using the alamar blue assay, and the degree of autophagy was determined microscopically. Mitochondrial respiration and glycolysis were measured simultaneously. The relative expression of autophagy-related genes BECN1, P62, BCL-2, and DRAM1 was determined by real-time PCR. HB affected cell growth, while starvation significantly increased the level of autophagy in the positive control compared to the basal level of autophagy in the untreated negative control. In HB-treated cultures, the degree of autophagy was higher compared to the basal level, and metabolic phenotypes were altered; both glycolysis and oxidative phosphorylation (OXPHOS) were decreased by HB at 0.2 and 0.4 mg/mL. Gene expression was deregulated towards autophagy induction and expansion. In conclusion, HB disrupted the bioenergetic metabolism and reduced the intracellular survival potential of BC cells. Further molecular studies are needed to confirm these findings and investigate their applicative potential. Full article

(This article belongs to the Topic Bioactive Compounds and Therapeutics: Molecular Aspects, Metabolic Profiles, and Omics Studies)

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12 pages, 3089 KiB

Open AccessArticle

Anaplerotic Therapy Using Triheptanoin in Two Brothers Suffering from Aconitase 2 Deficiency

by Maximilian Penkl, Johannes A. Mayr, René G. Feichtinger, Ralf Reilmann, Otfried Debus, Manfred Fobker, Anja Penkl, Janine Reunert, Stephan Rust and Thorsten Marquardt

Metabolites 2024, 14(4), 238; https://doi.org/10.3390/metabo14040238 - 20 Apr 2024

Viewed by 1374

Abstract

Citric acid cycle deficiencies are extremely rare due to their central role in energy metabolism. The ACO2 gene encodes the mitochondrial isoform of aconitase (aconitase 2), the second enzyme of the citric acid cycle. Approximately 100 patients with aconitase 2 deficiency have been [...] Read more.

Citric acid cycle deficiencies are extremely rare due to their central role in energy metabolism. The ACO2 gene encodes the mitochondrial isoform of aconitase (aconitase 2), the second enzyme of the citric acid cycle. Approximately 100 patients with aconitase 2 deficiency have been reported with a variety of symptoms, including intellectual disability, hypotonia, optic nerve atrophy, cortical atrophy, cerebellar atrophy, and seizures. In this study, a homozygous deletion in the ACO2 gene in two brothers with reduced aconitase 2 activity in fibroblasts has been described with symptoms including truncal hypotonia, optic atrophy, hyperopia, astigmatism, and cerebellar atrophy. In an in vivo trial, triheptanoin was used to bypass the defective aconitase 2 and fill up the citric acid cycle. Motor abilities in both patients improved. Full article

(This article belongs to the Topic Bioactive Compounds and Therapeutics: Molecular Aspects, Metabolic Profiles, and Omics Studies)

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16 pages, 1908 KiB

Open AccessArticle

Hemp Seed Oil Inhibits the Adipogenicity of the Differentiation-Induced Human Mesenchymal Stem Cells through Suppressing the Cannabinoid Type 1 (CB1)

by Albatul S. Almousa, Pandurangan Subash-Babu, Ibrahim O. Alanazi, Ali A. Alshatwi, Huda Alkhalaf, Eman Bahattab, Atheer Alsiyah and Mohammad Alzahrani

Molecules 2024, 29(7), 1568; https://doi.org/10.3390/molecules29071568 - 31 Mar 2024

Viewed by 1751

Abstract

Central and peripheral mechanisms of the endocannabinoid system (ECS) favor energy intake and storage. The ECS, especially cannabidiol (CBD) receptors, controls adipocyte differentiation (hyperplasia) and lipid accumulation (hypertrophy) in adipose tissue. In white adipose tissue, cannabidiol receptor 1 (CB1) stimulation increases lipogenesis and [...] Read more.

Central and peripheral mechanisms of the endocannabinoid system (ECS) favor energy intake and storage. The ECS, especially cannabidiol (CBD) receptors, controls adipocyte differentiation (hyperplasia) and lipid accumulation (hypertrophy) in adipose tissue. In white adipose tissue, cannabidiol receptor 1 (CB1) stimulation increases lipogenesis and inhibits lipolysis; in brown adipose tissue, it decreases mitochondrial thermogenesis and biogenesis. This study compared the availability of phytocannabinoids [CBD and Δ9-tetrahydrocannabinol (THC)] and polyunsaturated fatty acids [omega 3 (ω3) and omega 6 (ω6)] in different hemp seed oils (HSO). The study also examined the effect of HSO on adipocyte lipid accumulation by suppressing cannabinoid receptors in adipogenesis-stimulated human mesenchymal stem cells (hMSCs). Most importantly, Oil-Red-O′ and Nile red tests showed that HSO induced adipogenic hMSC differentiation without differentiation agents. Additionally, HSO-treated cells showed increased peroxisome proliferator-activated receptor gamma (PPARγ) mRNA expression compared to controls (hMSC). HSO reduced PPARγ mRNA expression after differentiation media (DM) treatment. After treatment with HSO, DM-hMSCs had significantly lower CB1 mRNA and protein expressions than normal hMSCs. HSO treatment also decreased transient receptor potential vanilloid 1 (TRPV1), fatty acid amide hydrolase (FAAH), and monoacylglycerol lipase (MGL) mRNAs in hMSC and DM-hMSCs. HSO treatment significantly decreased CB1, CB2, TRPV1, and G-protein-coupled receptor 55 (GPCR55) protein levels in DM-hMSC compared to hMSC in western blot analysis. In this study, HSO initiated adipogenic differentiation in hMSC without DM, but it suppressed CB1 gene and protein expression, potentially decreasing adipocyte lipid accumulation and lipogenic enzymes. Full article

(This article belongs to the Topic Bioactive Compounds and Therapeutics: Molecular Aspects, Metabolic Profiles, and Omics Studies)

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18 pages, 3191 KiB

Open AccessArticle

Dietary Methionine Restriction Improves Gut Health and Alters the Plasma Metabolomic Profile in Rats by Modulating the Composition of the Gut Microbiota

by Mei Yang, Qian Xie, Yintao Xiao, Minglong Xia, Jiashun Chen, Bi-E Tan and Yulong Yin

Int. J. Mol. Sci. 2024, 25(7), 3657; https://doi.org/10.3390/ijms25073657 - 25 Mar 2024

Viewed by 1803

Abstract

Dietary methionine restriction (MetR) offers an integrated set of beneficial health effects, including delaying aging, extending health span, preventing fat accumulation, and reducing oxidative stress. This study aimed to investigate whether MetR exerts entero-protective effects by modulating intestinal flora, and the effect of [...] Read more.

Dietary methionine restriction (MetR) offers an integrated set of beneficial health effects, including delaying aging, extending health span, preventing fat accumulation, and reducing oxidative stress. This study aimed to investigate whether MetR exerts entero-protective effects by modulating intestinal flora, and the effect of MetR on plasma metabolites in rats. Rats were fed diets containing 0.86% methionine (CON group) and 0.17% methionine (MetR group) for 6 weeks. Several indicators of inflammation, gut microbiota, plasma metabolites, and intestinal barrier function were measured. 16S rRNA gene sequencing was used to analyze the cecal microbiota. The MetR diet reduced the plasma and colonic inflammatory factor levels. The MetR diet significantly improved intestinal barrier function by increasing the mRNA expression of tight junction proteins, such as zonula occludens (ZO)-1, claudin-3, and claudin-5. In addition, MetR significantly increased the levels of short-chain fatty acids (SCFAs) by increasing the abundance of SCFAs-producing Erysipclotxichaceae and Clostridium_sensu_stricto_1 and decreasing the abundance of pro-inflammatory bacteria Proteobacteria and Escherichia-Shigella. Furthermore, MetR reduced the plasma levels of taurochenodeoxycholate-7-sulfate, taurocholic acid, and tauro-ursodeoxycholic acid. Correlation analysis identified that colonic acetate, total colonic SCFAs, 8-acetylegelolide, collettiside I, 6-methyladenine, and cholic acid glucuronide showed a significant positive correlation with Clostridium_sensu_stricto_1 abundance but a significant negative correlation with Escherichia-Shigella and Enterococcus abundance. MetR improved gut health and altered the plasma metabolic profile by regulating the gut microbiota in rats. Full article

(This article belongs to the Topic Bioactive Compounds and Therapeutics: Molecular Aspects, Metabolic Profiles, and Omics Studies)

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14 pages, 2059 KiB

Open AccessArticle

Overexpression of S30 Ribosomal Protein Leads to Transcriptional and Metabolic Changes That Affect Plant Development and Responses to Stress

by Alin Finkelshtein, Hala Khamesa-Israelov and Daniel A. Chamovitz

Biomolecules 2024, 14(3), 319; https://doi.org/10.3390/biom14030319 - 7 Mar 2024

Cited by 1 | Viewed by 1385

Abstract

ICT1 is an Arabidopsis thaliana line that overexpresses the gene encoding the S30 ribosomal subunit, leading to tolerance to exogenous indole-3-carbinol. Indole-3-carbinol (I3C) is a protective chemical formed as a breakdown of I3M in cruciferous vegetables. The overexpression of S30 in ICT1 results [...] Read more.

ICT1 is an Arabidopsis thaliana line that overexpresses the gene encoding the S30 ribosomal subunit, leading to tolerance to exogenous indole-3-carbinol. Indole-3-carbinol (I3C) is a protective chemical formed as a breakdown of I3M in cruciferous vegetables. The overexpression of S30 in ICT1 results in transcriptional changes that prime the plant for the I3C, or biotic insult. Emerging evidence suggests that ribosomal proteins play important extra-ribosomal roles in various biochemical and developmental processes, such as transcription and stress resistance. In an attempt to elucidate the mechanism leading to I3C and stress resistance in ICT1, and using a multi-pronged approach employing transcriptomics, metabolomics, phenomics, and physiological studies, we show that overexpression of S30 leads to specific transcriptional alterations, which lead to both changes in metabolites connected to biotic and oxidative stress tolerance and, surprisingly, to photomorphogenesis. Full article

(This article belongs to the Topic Bioactive Compounds and Therapeutics: Molecular Aspects, Metabolic Profiles, and Omics Studies)

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19 pages, 7200 KiB

Open AccessArticle

Optimization of Fermentation Process for New Anti-Inflammatory Glycosylceramide Metabolite from Aspergillus sp.

by Yung-Husan Chen, Qiaoqiao Zhu, Jingyi Li, Rong Yang, Jingwen Zhang, Minxin You, Lianzhong Luo and Bingye Yang

Metabolites 2024, 14(2), 99; https://doi.org/10.3390/metabo14020099 - 31 Jan 2024

Cited by 1 | Viewed by 1598

Abstract

A novel ceramide compound, named Aspercerebroside A (AcA), was successfully isolated from the ethyl acetate layer of the marine symbiotic fungus Aspergillus sp. AcA exhibited notable anti-inflammatory activity by effectively inhibiting the production of nitric oxide (NO) in RAW 264.7 cells at concentrations [...] Read more.

A novel ceramide compound, named Aspercerebroside A (AcA), was successfully isolated from the ethyl acetate layer of the marine symbiotic fungus Aspergillus sp. AcA exhibited notable anti-inflammatory activity by effectively inhibiting the production of nitric oxide (NO) in RAW 264.7 cells at concentrations of 30 μg/mL and 40 μg/mL, offering a promising avenue for the treatment of inflammatory diseases. To optimize the yield of glycosylceramide (AcA), a series of techniques, including single-factor experiments, orthogonal experiments, and response surface optimization, were systematically employed to fine-tune the composition of the fermentation medium. Initially, the optimal carbon source (sucrose), nitrogen source (yeast extract powder), and the most suitable medium salinity (14 ppt) were identified through single-factor experiments. Subsequently, orthogonal experiments, employing an orthogonal table for planning and analyzing multifactor experiments, were conducted. Finally, a mathematical model, established using a Box–Behnken design, comprehensively analyzed the interactions between the various factors to determine the optimal composition of the fermentation medium. According to the model’s prediction, when the sucrose concentration was set at 37.47 g/L, yeast extract powder concentration at 19.66 g/L, and medium salinity at 13.31 ppt, the predicted concentration of glycosylceramide was 171.084 μg/mL. The experimental results confirmed the model’s accuracy, with the actual average concentration of glycosylceramide under these conditions measured at 171.670 μg/mL, aligning closely with the predicted value. Full article

(This article belongs to the Topic Bioactive Compounds and Therapeutics: Molecular Aspects, Metabolic Profiles, and Omics Studies)

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18 pages, 2370 KiB

Open AccessReview

G-Quadruplexes in Human Telomere: Structures, Properties, and Applications

by Yan Xu and Makoto Komiyama

Molecules 2024, 29(1), 174; https://doi.org/10.3390/molecules29010174 - 27 Dec 2023

Cited by 4 | Viewed by 2740

Abstract

G-quadruplexes, intricate four-stranded structures composed of G-tetrads formed by four guanine bases, are prevalent in both DNA and RNA. Notably, these structures play pivotal roles in human telomeres, contributing to essential cellular functions. Additionally, the existence of DNA:RNA hybrid G-quadruplexes adds a layer [...] Read more.

G-quadruplexes, intricate four-stranded structures composed of G-tetrads formed by four guanine bases, are prevalent in both DNA and RNA. Notably, these structures play pivotal roles in human telomeres, contributing to essential cellular functions. Additionally, the existence of DNA:RNA hybrid G-quadruplexes adds a layer of complexity to their structural diversity. This review provides a comprehensive overview of recent advancements in unraveling the intricacies of DNA and RNA G-quadruplexes within human telomeres. Detailed insights into their structural features are presented, encompassing the latest developments in chemical approaches designed to probe these G-quadruplex structures. Furthermore, this review explores the applications of G-quadruplex structures in targeting human telomeres. Finally, the manuscript outlines the imminent challenges in this evolving field, setting the stage for future investigations. Full article

(This article belongs to the Topic Bioactive Compounds and Therapeutics: Molecular Aspects, Metabolic Profiles, and Omics Studies)

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16 pages, 3722 KiB

Open AccessArticle

Absorption, Distribution, Metabolism, and Excretion of [¹⁴C]BS1801, a Selenium-Containing Drug Candidate, in Rats

by Cheng Yang, Mingzhen Xue, Yifei He, Hanwei Yin, Chen Yang, Dafang Zhong, Huihui Zeng, Yuandong Zheng and Xingxing Diao

Molecules 2023, 28(24), 8102; https://doi.org/10.3390/molecules28248102 - 15 Dec 2023

Cited by 1 | Viewed by 1172

Abstract

BS1801 is a selenium-containing drug candidate with potential for treating liver and lung fibrosis. To fully elucidate the biotransformation of BS1801 in animals and provide sufficient preclinical drug metabolism data for human mass balance study, the metabolism of BS1801 in rats was investigated. [...] Read more.

BS1801 is a selenium-containing drug candidate with potential for treating liver and lung fibrosis. To fully elucidate the biotransformation of BS1801 in animals and provide sufficient preclinical drug metabolism data for human mass balance study, the metabolism of BS1801 in rats was investigated. We used radiolabeling techniques to investigate the mass balance, tissue distribution, and metabolite identification of BS1801 in Sprague–Dawley/Long–Evans rats after a single oral dose of 100 mg/kg (100 μCi/kg) [¹⁴C]BS1801: 1. The mean recovery of radioactive substances in urine and feces was 93.39% within 168 h postdose, and feces were the main excretion route. 2. Additionally, less than 1.00% of the dose was recovered from either urine or bile. 3. BS1801-related components were widely distributed throughout the body. 4. Fifteen metabolites were identified in rat plasma, urine, feces, and bile, and BS1801 was detected only in feces. 5. BS1801-M484, the methylation product obtained via a N–Se bond reduction in BS1801, was the most abundant drug-related component in plasma. The main metabolic pathways of BS1801 were reduction, amide hydrolysis, oxidation, and methylation. Overall, BS1801 was distributed throughout the body, and excreted mainly as an intact BS1801 form through feces. No differences were observed between male and female rats in distribution, metabolism, and excretion of BS1801. Full article

(This article belongs to the Topic Bioactive Compounds and Therapeutics: Molecular Aspects, Metabolic Profiles, and Omics Studies)

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22 pages, 7459 KiB

Open AccessArticle

Rhododendron chrysanthum’s Primary Metabolites Are Converted to Phenolics More Quickly When Exposed to UV-B Radiation

by Fushuai Gong, Wang Yu, Qingpan Zeng, Jiawei Dong, Kun Cao, Hongwei Xu and Xiaofu Zhou

Biomolecules 2023, 13(12), 1700; https://doi.org/10.3390/biom13121700 - 24 Nov 2023

Cited by 10 | Viewed by 1289

Abstract

The plant defense system is immediately triggered by UV-B irradiation, particularly the production of metabolites and enzymes involved in the UV-B response. Although substantial research on UV-B-related molecular responses in Arabidopsis has been conducted, comparatively few studies have examined the precise consequences of [...] Read more.

The plant defense system is immediately triggered by UV-B irradiation, particularly the production of metabolites and enzymes involved in the UV-B response. Although substantial research on UV-B-related molecular responses in Arabidopsis has been conducted, comparatively few studies have examined the precise consequences of direct UV-B treatment on R. chrysanthum. The ultra-high-performance liquid chromatography tandem mass spectrometry (UPLC-MS/MS) methodology and TMT quantitative proteomics are used in this study to describe the metabolic response of R. chrysanthum to UV-B radiation and annotate the response mechanism of the primary metabolism and phenolic metabolism of R. chrysanthum. The outcomes demonstrated that following UV-B radiation, the primary metabolites (L-phenylalanine and D-lactose*) underwent considerable changes to varying degrees. This gives a solid theoretical foundation for investigating the use of precursor substances, such as phenylalanine, to aid plants in overcoming abiotic stressors. The external application of ABA produced a considerable increase in the phenolic content and improved the plants’ resistance to UV-B damage. Our hypothesis is that externally applied ABA may work in concert with UV-B to facilitate the transformation of primary metabolites into phenolic compounds. This hypothesis offers a framework for investigating how ABA can increase a plant’s phenolic content in order to help the plant withstand abiotic stressors. Overall, this study revealed alterations and mechanisms of primary and secondary metabolic strategies in response to UV-B radiation. Full article

(This article belongs to the Topic Bioactive Compounds and Therapeutics: Molecular Aspects, Metabolic Profiles, and Omics Studies)

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21 pages, 8880 KiB

Open AccessArticle

Unravelling Effects of Rosemary (Rosmarinus officinalis L.) Extract on Hepatic Fat Accumulation and Plasma Lipid Profile in Rats Fed a High-Fat Western-Style Diet

by Sidsel Madsen, Steffen Yde Bak, Christian Clement Yde, Henrik Max Jensen, Tine Ahrendt Knudsen, Cecilie Bæch-Laursen, Jens Juul Holst, Christoffer Laustsen and Mette Skou Hedemann

Metabolites 2023, 13(9), 974; https://doi.org/10.3390/metabo13090974 - 27 Aug 2023

Cited by 2 | Viewed by 2217

Abstract

The objective of the study was to investigate the preventive effect on obesity-related conditions of rosemary (Rosmarinus officinalis L.) extract (RE) in young, healthy rats fed a high-fat Western-style diet to complement the existing knowledge gap concerning the anti-obesity effects of RE [...] Read more.

The objective of the study was to investigate the preventive effect on obesity-related conditions of rosemary (Rosmarinus officinalis L.) extract (RE) in young, healthy rats fed a high-fat Western-style diet to complement the existing knowledge gap concerning the anti-obesity effects of RE in vivo. Sprague Dawley rats (71.3 ± 0.46 g) were fed a high-fat Western-style diet (WD) or WD containing either 1 g/kg feed or 4 g/kg feed RE for six weeks. A group fed standard chow served as a negative control. The treatments did not affect body weight; however, the liver fat percentage was reduced in rats fed RE, and NMR analyses of liver tissue indicated that total cholesterol and triglycerides in the liver were reduced. In plasma, HDL cholesterol was increased while triglycerides were decreased. Rats fed high RE had significantly increased fasting plasma concentrations of Glucagon-like peptide-1 (GLP-1). Proteomics analyses of liver tissue showed that RE increased enzymes involved in fatty acid oxidation, possibly associated with the higher fasting GLP-1 levels, which may explain the improvement of the overall lipid profile and hepatic fat accumulation. Furthermore, high levels of succinic acid in the cecal content of RE-treated animals suggested a modulation of the microbiota composition. In conclusion, our results suggest that RE may alleviate the effects of consuming a high-fat diet through increased GLP-1 secretion and changes in microbiota composition. Full article

(This article belongs to the Topic Bioactive Compounds and Therapeutics: Molecular Aspects, Metabolic Profiles, and Omics Studies)

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13 pages, 2178 KiB

Open AccessArticle

Novel Quinazoline Derivative Induces Differentiation of Keratinocytes and Enhances Skin Barrier Functions against Th2 Cytokine-Mediated Signaling

by Yukyung Park, Huddar Srigouri and Dongwon Kim

Molecules 2023, 28(16), 6119; https://doi.org/10.3390/molecules28166119 - 18 Aug 2023

Cited by 1 | Viewed by 1507

Abstract

Atopic dermatitis (AD) is a common inflammatory skin disease characterized by pruritic lesions and skin barrier dysfunction. In this study, we evaluated the effect of a quinazoline derivative, SH-340, on TSLP expression and signaling in human primary keratinocytes. Our results demonstrated that SH-340 [...] Read more.

Atopic dermatitis (AD) is a common inflammatory skin disease characterized by pruritic lesions and skin barrier dysfunction. In this study, we evaluated the effect of a quinazoline derivative, SH-340, on TSLP expression and signaling in human primary keratinocytes. Our results demonstrated that SH-340 significantly increased factors for differentiation and skin barrier function including KRT1, KRT2, KRT10, IVL, LOR, CLDN1, OVOL1, and FLG, whereas it inhibited TSLP expression in a dose-dependent manner, both at the mRNA and protein levels. Furthermore, SH-340 was found to inhibit the phosphorylation of STAT6, a downstream signaling molecule of IL-4 and IL-13, in keratinocytes. These findings suggest that SH-340 may suppress TSLP expression by inhibiting the IL-4/IL-13-STAT6 signaling pathway. Finally, SH-340 may potentially contribute to both the alleviation of inflammation and the restoration of skin barrier function. Full article

(This article belongs to the Topic Bioactive Compounds and Therapeutics: Molecular Aspects, Metabolic Profiles, and Omics Studies)

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15 pages, 2557 KiB

Open AccessReview

Research Progress of Takeda G Protein-Coupled Receptor 5 in Metabolic Syndrome

by Xianmei Gou, Lin Qin, Di Wu, Jian Xie, Yanliu Lu, Qianru Zhang and Yuqi He

Molecules 2023, 28(15), 5870; https://doi.org/10.3390/molecules28155870 - 4 Aug 2023

Cited by 7 | Viewed by 2666

Abstract

Bile acids are acknowledged as signaling molecules involved in metabolic syndrome. The Takeda G protein-coupled receptor 5 (TGR5) functions as a significant bile acid receptor. The accumulated evidence suggests that TGR5 involves lipid homeostasis, glucose metabolism, and inflammation regulation. In line with this, [...] Read more.

Bile acids are acknowledged as signaling molecules involved in metabolic syndrome. The Takeda G protein-coupled receptor 5 (TGR5) functions as a significant bile acid receptor. The accumulated evidence suggests that TGR5 involves lipid homeostasis, glucose metabolism, and inflammation regulation. In line with this, recent preclinical studies also demonstrate that TGR5 plays a significant role in the generation and progression of metabolic syndrome, encompassing type 2 diabetes mellitus, obesity, atherosclerosis, and non-alcoholic fatty liver disease (NAFLD). In this review, we discuss the role of TGR5 in metabolic syndrome, illustrating the underlying mechanisms and therapeutic targets. Full article

(This article belongs to the Topic Bioactive Compounds and Therapeutics: Molecular Aspects, Metabolic Profiles, and Omics Studies)

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19 pages, 6514 KiB

Open AccessArticle

Mucosal Metabolomic Signatures in Chronic Colitis: Novel Insights into the Pathophysiology of Inflammatory Bowel Disease

by Nathan Calzadilla, Aisha Qazi, Anchal Sharma, Kai Mongan, Shane Comiskey, Jahnavi Manne, Alvin G. Youkhana, Sonam Khanna, Seema Saksena, Pradeep K. Dudeja, Waddah A. Alrefai and Ravinder K. Gill

Metabolites 2023, 13(7), 873; https://doi.org/10.3390/metabo13070873 - 23 Jul 2023

Cited by 4 | Viewed by 2167

Abstract

Inflammatory bowel diseases (IBD) involve complex interactions among genetic factors, aberrant immune activation, and gut microbial dysbiosis. While metabolomic studies have focused on feces and serum, fewer investigations have examined the intestinal mucosa despite its crucial role in metabolite absorption and transport. The [...] Read more.

Inflammatory bowel diseases (IBD) involve complex interactions among genetic factors, aberrant immune activation, and gut microbial dysbiosis. While metabolomic studies have focused on feces and serum, fewer investigations have examined the intestinal mucosa despite its crucial role in metabolite absorption and transport. The goals of this study were twofold: to test the hypothesis that gut microbial dysbiosis from chronic intestinal inflammation leads to mucosal metabolic alterations suitable for therapeutic targeting, and to address gaps in metabolomic studies of intestinal inflammation that have overlooked the mucosal metabolome. The chronic DSS colitis was induced for five weeks in 7–9-week-old wild-type C57BL/6J male mice followed by microbial profiling with targeted 16srRNA sequencing service. Mucosal metabolite measurements were performed by Metabolon (Morrisville, NC). The data were analyzed using the bioinformatic tools Pathview, MetOrigin, and Metaboanalyst. The novel findings demonstrated increases in several host- and microbe-derived purine, pyrimidine, endocannabinoid, and ceramide metabolites in colitis. Origin analysis revealed that microbial-related tryptophan metabolites kynurenine, anthranilate, 5-hydroxyindoleacetate, and C-glycosyltryptophan were significantly increased in colon mucosa during chronic inflammation and strongly correlated with disease activity. These findings offer new insights into the pathophysiology of IBD and provide novel potential targets for microbial-based therapeutics. Full article

(This article belongs to the Topic Bioactive Compounds and Therapeutics: Molecular Aspects, Metabolic Profiles, and Omics Studies)

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18 pages, 2539 KiB

Open AccessArticle

Identification of Small Molecules Affecting the Secretion of Therapeutic Antibodies with the Retention Using Selective Hook (RUSH) System

by Mathilde Coulet, Sylvie Lachkar, Marion Leduc, Marc Trombe, Zelia Gouveia, Franck Perez, Oliver Kepp, Guido Kroemer and Stéphane Basmaciogullari

Cells 2023, 12(12), 1642; https://doi.org/10.3390/cells12121642 - 16 Jun 2023

Viewed by 2378

Abstract

Unlocking cell secretion capacity is of paramount interest for the pharmaceutical industry focused on biologics. Here, we leveraged retention using a selective hook (RUSH) system for the identification of human osteosarcoma U2OS cell secretion modulators, through automated, high-throughput screening of small compound libraries. [...] Read more.

Unlocking cell secretion capacity is of paramount interest for the pharmaceutical industry focused on biologics. Here, we leveraged retention using a selective hook (RUSH) system for the identification of human osteosarcoma U2OS cell secretion modulators, through automated, high-throughput screening of small compound libraries. We created a U2OS cell line which co-expresses a variant of streptavidin addressed to the lumen-facing membrane of the endoplasmic reticulum (ER) and a recombinant anti-PD-L1 antibody. The heavy chain of the antibody was modified at its C-terminus, to which a furin cleavage site, a green fluorescent protein (GFP), and a streptavidin binding peptide (SBP) were added. We show that the U2OS cell line stably expresses the streptavidin hook and the recombinant antibody bait, which is retained in the ER through the streptavidin–SBP interaction. We further document that the addition of biotin to the culture medium triggers the antibody release from the ER, its trafficking through the Golgi where the GFP-SBP moiety is clipped off, and eventually its release in the extra cellular space, with specific antigen-binding properties. The use of this clone in screening campaigns led to the identification of lycorine as a secretion enhancer, and nigericin and tyrphostin AG-879 as secretion inhibitors. Altogether, our data support the utility of this approach for the identification of agents that could be used to improve recombinant production yields and also for a better understanding of the regulatory mechanism at work in the conventional secretion pathway. Full article

(This article belongs to the Topic Bioactive Compounds and Therapeutics: Molecular Aspects, Metabolic Profiles, and Omics Studies)

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21 pages, 3669 KiB

Open AccessArticle

Ginsentide TP1 Protects Hypoxia-Induced Dysfunction and ER Stress-Linked Apoptosis

by Bamaprasad Dutta, Shining Loo, Antony Kam, Siu Kwan Sze and James P. Tam

Cells 2023, 12(10), 1401; https://doi.org/10.3390/cells12101401 - 16 May 2023

Cited by 4 | Viewed by 2843

Abstract

Hypoxia-induced vascular endothelial dysfunction (VED) is a significant contributor to several severe human diseases, including heart disease, stroke, dementia, and cancer. However, current treatment options for VED are limited due to the lack of understanding of the underlying disease mechanisms and therapeutic leads. [...] Read more.

Hypoxia-induced vascular endothelial dysfunction (VED) is a significant contributor to several severe human diseases, including heart disease, stroke, dementia, and cancer. However, current treatment options for VED are limited due to the lack of understanding of the underlying disease mechanisms and therapeutic leads. We recently discovered a heat-stable microprotein in ginseng, called ginsentide TP1, that has been shown to reduce vascular dysfunction in cardiovascular disease models. In this study, we use a combination of functional assays and quantitative pulsed SILAC proteomics to identify new proteins synthesized in hypoxia and to show that ginsentide TP1 provides protection for human endothelial cells against hypoxia and ER stress. Consistent with the reported findings, we also found that hypoxia activates various pathways related to endothelium activation and monocyte adhesion, which in turn, impairs nitric oxide (NO) synthase activity, reduces the bioavailability of NO, and increases the production of reactive oxygen species that contribute to VED. Additionally, hypoxia triggers endoplasmic reticulum stress and initiates apoptotic signaling pathways associated with cardiovascular pathology. Treatment with ginsentide TP1 reduced surface adhesion molecule expression, prevented activation of the endothelium and leukocyte adhesion, restored protein hemostasis, and reduced ER stress to protect against hypoxia-induced cell death. Ginsentide TP1 also restored NO signaling and bioavailability, reduced oxidative stress, and protected endothelial cells from endothelium dysfunction. In conclusion, this study shows that the molecular pathogenesis of VED induced by hypoxia can be mitigated by treatment with ginsentide TP1, which could be one of the key bioactive compounds responsible for the “cure-all” effect of ginseng. This research may lead to the development of new therapies for cardiovascular disorders. Full article

(This article belongs to the Topic Bioactive Compounds and Therapeutics: Molecular Aspects, Metabolic Profiles, and Omics Studies)

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