Search Results (271)

In this study, polysaccharides from Ficus carica L. fruits (FCPs) were extracted using a deep eutectic solvent (DES)-based ultrasound-assisted extraction (UAE) method. The physicochemical properties of the FCPs were then characterized, and the anti-aging effects of FCPs were evaluated in Caenorhabditis elegans (C. elegans). It was demonstrated that FCPs significantly extended the lifespan of the nematodes, while improving locomotor activity without affecting the body size or reproductive capacity. Meanwhile, FCPs reduced lipofuscin accumulation, decreased intracellular reactive oxygen species (ROS) levels, and increased the survival of C. elegans under oxidative stress. Moreover, FCPs upregulated the expression of antioxidant genes sod-1, sod-3, ctl-2, ctl-3 and gst-4. The expression of skinhead-1 (skn-1), a homologue gene of mammalian nuclear factor erythroid 2-related factor (Nrf) in C. elegans, was also elevated upon FCPs treatment. Knockdown of skn-1 expression by RNA interference abolished the lifespan extension and ROS reduction in FCPs-treated C. elegans, indicating that the SKN-1-mediated signaling was essential for the anti-aging effects of FCPs. Additionally, FCPs caused downregulation of the key components of the insulin/IGF-1 signaling (IIS) pathway, age-1, akt-1, and akt-2. Overall, these results suggested that FCPs promoted longevity in C. elegans via modulation of SKN-1 and IIS pathway. Full article

Atherosclerosis is a chronic inflammatory arterial disease and the primary underlying cause of cardiovascular morbidity and mortality worldwide. Its development and progression are driven by a mechanistically interconnected triad of endothelial dysfunction, oxidative stress, and vascular inflammation. Current pharmacotherapy, primarily focused on low-density lipoprotein cholesterol (LDL-C) reduction through statin-based and adjunctive therapies, does not fully address the residual inflammatory and calcific components of atherosclerotic risk. Menaquinone-7 (MK-7), a long-chain isoform of vitamin K2 with superior bioavailability and extrahepatic tissue distribution, has emerged as a multi-target modulator of atherogenic processes. Its classical function is to serve as a cofactor for the gamma-carboxylation of vitamin K-dependent proteins (VKDPs), principally matrix Gla protein (MGP), the primary endogenous inhibitor of vascular calcification. Beyond this established pathway, a growing body of experimental evidence indicates that MK-7 may modulate endothelial nitric oxide (NO) production through carboxylation-dependent activation of Growth Arrest-Specific Protein 6 (Gas6) and suppress lipid peroxidation and ferroptosis via Ferroptosis Suppressor Protein 1 (FSP1)-mediated reduction of vitamin K hydroquinone (VKH₂). In addition, it may attenuate nuclear factor kappa-B (NF-κB)-driven inflammatory gene transcription in vascular cells. Previous reviews mainly focused on how vitamin K2 influences vascular calcification and cardiovascular outcomes. However, emerging mechanistic evidence linking MK-7 to endothelial dysfunction, oxidative stress, ferroptosis, and vascular inflammation has not been comprehensively integrated. This review summarizes the current knowledge of in vitro, animal, observational, and randomized controlled trial evidence for MK-7 in the context of atherosclerosis. It particularly emphasises mechanistic pathways, the strength of evidence, and translational limitations, highlighting the lack of direct human vascular evidence in several areas. Full article

Plants frequently encounter overlapping, sequential, and recurrent stresses, but the cellular mechanisms that organize responses to these complex conditions remain incompletely understood. Biomolecular condensates are membrane-less assemblies formed through phase separation and multivalent molecular interactions, and they can regulate RNA metabolism, protein sequestration, signaling specificity, transcriptional control, and stress recovery. This review evaluates the hypothesis that plant condensates may contribute to the organization of combined and recurrent stress responses by modulating molecular accessibility, transcript fate, proteostasis, and regulatory crosstalk. We synthesize current knowledge on stress granules, processing bodies, nuclear condensates, plastid-associated condensate-like assemblies, and other stress-responsive compartments, with emphasis on their possible roles in signal filtering, RNA triage, and recovery-associated reprogramming. We also distinguish established evidence from emerging hypotheses, particularly regarding condensate-mediated signal prioritization and stress memory. Current data support condensates as rapid stress-responsive organizers, but direct evidence for their persistence after recovery or their causal roles under simultaneous multi-stress conditions remains limited. By integrating phase separation biology with plant multi-stress physiology, this review proposes a testable conceptual framework and identifies methodological priorities for future studies in plant stress resilience and crop improvement. Full article

Endurance training camps are well established in elite sports, but one-week camps for recreational endurance athletes have recently gained popularity despite limited scientific evidence. This study investigated the effects of a one-week endurance training camp on body composition, endurance performance, and markers of metabolic stress and mitochondrial adaptation in recreational athletes. Female and male endurance athletes (≥18 years) participated in a professionally guided one-week endurance training camp. Assessments included body composition, running diagnostics, sleep-quality/recovery-stress questionnaires, nutrition/energy balance diaries, blood profiling, and mitochondrial biogenesis markers. Measurements were conducted before (pre), during (camp), and after the camp (post). A total of 35 participants (18 male/17 female) were included. Body mass and body fat decreased from pre- to post-camp. Lactate concentrations at threshold levels changed, while velocities at fixed lactate concentrations and maximal oxygen uptake did not significantly improve. Post-camp, lactate dehydrogenase, klotho, and vitamin D increased, whereas interferon-γ, kynurenine, cortisol, creatinine, and ferritin decreased. Plasma mitochondrial and nuclear DNA abundance, as well as PGC1-α expression, increased, while vascular endothelial growth factor decreased. A one-week endurance training camp in a holiday-like setting induces measurable physiological, metabolic, and mitochondrial adaptations in recreational athletes and is associated with reduced systemic and psychological stress. However, the concurrent increase in muscle- and cell-stress markers indicates a substantial physiological load. Full article

Cadmium (Cd) is a typical heavy metal pollutant in aquatic environments. It enters fish through the gills, digestive tract, and body surface, and accumulates mainly in the liver and kidneys, with species- and tissue-specific distribution. Cadmium triggers apoptosis by inducing oxidative stress, calcium imbalance, and DNA damage. These signals are integrated and amplified by the mitogen-activated protein kinase (MAPK), nuclear factor kappa B (NF-κB), phosphatidylinositol 3-kinase (PI3K)/AKT, and nuclear factor erythroid 2-related factor 2 (Nrf2) pathways, ultimately activating three downstream apoptotic execution pathways: the death receptor, mitochondrial, and endoplasmic reticulum stress pathways. These three pathways form an interactive network through molecular nodes such as BH3 interacting domain death agonist (Bid), Ca²⁺, c-Jun N-terminal kinase (JNK), and C/EBP homologous protein (CHOP), synergistically amplifying the apoptotic effect, with the mitochondrial pathway playing a central role. Cadmium-induced apoptosis is dose-dependent: low concentrations activate protective responses, whereas high concentrations strongly promote apoptosis. Current research gaps remain regarding dynamic pathway crosstalk, chronic low-dose effects, species differences, and fish-specific apoptotic molecules (e.g., caspase-12 homologs). Future studies should focus on constructing multidimensional response maps, clarifying pathway activation thresholds and interaction contributions, and developing composite protective strategies based on Nrf2 activators, metal chelators, and antioxidants, thereby promoting translation into ecological risk assessment and aquaculture pollution control. Full article

Metabolic dysfunction-associated fatty liver disease (MAFLD) is the most prevalent chronic liver disease worldwide with complex pathogenesis and no approved specific therapy. Siraitia grosvenorii is a widely used medicinal and edible herb, yet its efficacy and underlying mechanisms against MAFLD remain poorly defined. This study explored the protective effects and potential mechanisms of aqueous extract of Siraitia grosvenorii (AESG) on MAFLD. Based on ultra-high-performance liquid chromatography-linear trap quadrupole orbitrap mass spectrometry (UHPLC-LTQ-Orbitrap-MS) analysis, 38 components in AESG were tentatively assigned, with tetracyclic triterpene saponins being the most abundant. In high-fat diet (HFD)-induced MAFLD mice, AESG significantly attenuated body weight gain, reduced plasma total cholesterol (T-CHO) and low-density lipoprotein cholesterol (LDL-C) levels, and dramatically decreased hepatic triglyceride (TG) accumulation from 0.0141 mmol/g in the model group to 0.0063 mmol/g in the low-dose AESG group, corresponding to a reduction of 55.00%. AESG also alleviated plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, and improved hepatocyte steatosis. Furthermore, AESG restored HFD-induced gut dysbiosis by enriching beneficial bacteria including Akkermansia and suppressing harmful bacteria such as Ruminococcus. In free fatty acids (FFA) stimulated HepG2 cells, AESG suppressed de novo lipogenesis via downregulating Fatty Acid Synthase (FASN), Acetyl-CoA Carboxylase (ACC) and Sterol Regulatory Element-Binding Protein 1c (SREBP1c), and enhanced antioxidant capacity via activating the Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2)/Heme Oxygenase 1 (HO-1)/Sirtuin 1 (SIRT1) pathway, thereby attenuating lipid accumulation and oxidative stress. In conclusion, AESG ameliorates MAFLD by inhibiting lipogenesis, improving oxidative stress, and regulating gut microbiota. These findings support Siraitia grosvenorii as a promising natural dietary intervention for MAFLD prevention and adjuvant therapy. Full article

Oxidative stress disrupts protein function through direct oxidation and triggers adaptive post-translational modifications. Among these, small ubiquitin-like modifier (SUMO)-ylation mediates fast and reversible remodeling of nuclear and cytoplasmic proteins. Redox regulation of the SUMO E1–E2 conjugation complex and specific SUMO proteases, such as SENP1 and SENP3, allows ROS to influence SUMO turnover and substrate selectivity. This defines SUMOylation as a versatile stress-response module under oxidative stress. In this review, we describe oxidative stress-induced remodeling of SUMO conjugation and deconjugation, with a focus on SUMO2/3 responses that transiently adjust transcription, DNA damage repair, and nuclear body dynamics. We discuss disease-relevant SUMO targets and pathological alterations in SUMO regulation across four major disease categories: neurodegenerative diseases, cardiovascular disease, cancer, and diabetes/metabolic diseases. In addition, we summarize emerging evidence connecting redox-sensitive SUMO remodeling to germ-cell function and reproductive health. Together, these perspectives highlight the dual role of SUMOylation as both a driver of stress adaptation and a tractable target for informing therapeutic strategies targeting the SUMO pathway. Full article

Prostate cancer (PCa) progression is critically driven by androgen receptor (AR) signaling, which integrates hormonal cues with metabolic programs supporting tumor growth, survival, and therapy resistance. Emerging evidence suggests that intermittent fasting (IF) and related dietary interventions—such as time-restricted eating (TRE), alternate-day fasting (ADF), and fasting-mimicking diet (FMD)—modulate systemic metabolism, including reductions in insulin and insulin-like growth factor 1 (IGF-1), and induce intracellular nutrient stress that can influence AR activity, splice variant expression (e.g., AR-V7), and downstream metabolic pathways. This systematic literature review (Scopus, PubMed, Web of Science; publications up to December 2025; search terms: “prostate cancer,” “androgen receptor,” “AR splice variants,” “intermittent fasting,” “fasting mimicking diet”, “metabolism,” “therapy resistance”) summarizes preclinical and clinical studies addressing the impact of IF on AR signaling, lipogenesis, mitochondrial function, redox homeostasis, and therapy response. Preclinical studies indicate that IF can reduce AR expression, impair nuclear translocation, modulate AR splice variants such as AR-V7 via nutrient-sensitive splicing mechanisms, and enhance sensitivity to androgen deprivation therapy and AR-targeted agents. Mechanistically, IF-induced metabolic stress engages AMP-activated protein kinase (AMPK), mechanistic target of rapamycin (mTOR), and sirtuin pathways, alters lipid and mitochondrial metabolism, and transiently increases reactive oxygen species (ROS), creating vulnerabilities in prostate tumor cells. Translational evidence suggests potential benefits of integrating IF with standard therapy, but effects may depend on fasting regimen, caloric intake, macronutrient composition, and patient metabolic context, including risk of lean mass loss. This review highlights the metabolic crosstalk between IF and AR signaling and emphasizes the need for future clinical studies incorporating biomarker-guided approaches and body composition monitoring to fully exploit this intersection for improved therapeutic outcomes in prostate cancer. Full article

Heat stress (HS) severely impairs boar reproductive function by inducing oxidative stress and inflammatory responses, while lycopene (LYC), as a potent antioxidant, exerts a potential protective effect on the male reproductive system. This study aimed to clarify the mechanism underlying LYC-mediated alleviation of HS-induced decline in semen quality in Rongchang boars, identify the most affected tissues, and explore its regulatory role in the Nrf2 (Nuclear factor E2-related factor 2) pathway. A total of 18 Rongchang boars with an initial body weight of 15.81 ± 1.07 kg were randomly assigned to three groups (6 boars per group): the control group (CON, 26 ± 1 °C), the heat stress group (HS, exposed to 35 ± 1 °C for 8 h daily), and the heat stress + 100 mg/kg lycopene group (HS + LYC). After 28 days of adaptive feeding and 14 days of HS treatment, samples were collected for semen quality analysis, testicular histological analysis, antioxidant index detection, transcriptome analysis, Nrf2 pathway detection, and inflammatory index detection. The results showed that HS significantly increased the sperm abnormality rate (p < 0.05), damaged the testicular structure, and induced oxidative stress in serum, lung, liver, left ventricle, testis, and epididymis (caput epididymis, corpus epididymis, cauda epididymis), with varying degrees of oxidative stress observed in these samples. Among these tissues, the testis and cauda epididymis exhibited the most significant responses to HS and LYC, with the comprehensive impact magnitudes of 317% and 514%, respectively. Enrichment analysis of differentially expressed genes (DEGs) in these two tissues revealed that the pathways mediating oxidative stress response displayed distinct tissue specificity, and all of them were closely associated with the Nrf2 antioxidant signaling pathway. HS significantly downregulated the mRNA expressions of Nrf2, Quinone Oxidoreductase (NQO1), Heme Oxygenase 1 (HMOX1) and Glutamate-Cysteine Ligase Catalytic Subunit (GCLC) genes as well as the protein level of Nrf2 in the testis and cauda epididymis, increased the protein level of Keap1, and significantly elevated the levels of interleukin-6 (IL-6), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in these two tissues (p < 0.05). Compared with the HS group, dietary supplementation of LYC significantly improved sperm motility and the proportion of rapidly progressive sperm, reduced the proportion of immotile sperm and sperm abnormality rate (p < 0.05), alleviated testicular damage and oxidative stress in various tissues, upregulated the mRNA expressions of Nrf2 and HMOX1 genes in the testis as well as the mRNA expressions of Nrf2, NQO1, HMOX1 and GCLC genes in cauda epididymis (p < 0.05), significantly increased the Nrf2 protein level and decreased the Keap1 protein level in these two tissues, and simultaneously decreased the levels of the aforementioned inflammatory factors (p < 0.05). In conclusion, dietary supplementation with 100 mg/kg LYC can alleviate HS-induced decline in semen quality and testicular damage by regulating the oxidative status and inflammatory level of relevant tissues (e.g., testis and cauda epididymis) in boars, and this protective effect may be associated with the regulation of the Nrf2 signaling pathway. Full article

In vitro maturation (IVM) is highly susceptible to influences of the culture environment, which can lead to increased intracellular reactive oxygen species (ROS) levels and thereby induce a stress response in oocytes, ultimately reducing the developmental potential of early embryos. Brain-derived neurotrophic factor (BDNF) is an ovarian endocrine factor that can enhance the function of follicular granulosa cells and promote oocyte maturation, but the specific pathways remain unclear. We supplemented IVM cultures of sheep oocytes with BDNF and examined aspects of oocyte nuclear and cytoplasmic maturation. The addition of 50 ng/mL BDNF promoted the expansion of cumulus cells and increased the rates of first polar body extrusion, cleavage, and blastocyst formation. Compared with untreated controls, BDNF-treated oocytes had improved Ca²⁺ homeostasis, enhanced expression of antioxidant genes, decreased ROS levels and expression of endoplasmic reticulum stress genes, and increased mitochondrial membrane potential, mitochondrial biogenesis, and numbers of cells with proper distributions of mitochondria and endoplasmic reticulum. Further analysis indicated that BDNF affected oocyte maturation by increasing the numbers of transzonal projections and gap junctions during the IVM process. In summary, the addition of BDNF during the IVM process improved sheep oocyte maturation and embryo development by reducing oxidative stress and endoplasmic reticulum stress. These findings deepen our understanding of the regulatory mechanisms of BDNF during IVM and provide experimental data to improve in vitro embryo production from sheep oocytes. Full article

The Japanese beetle (Popillia japonica Newman) is a highly invasive, polyphagous scarab causing significant agricultural and ecological damage across invaded regions. While molecular studies are gaining traction, the unavailability of P. japonica cell lines has constrained in vitro investigations. To overcome these limitations and provide a platform for controlled biological investigation, we developed the first cell culture derived from P. japonica larvae. Fat bodies from field-collected third-instar larvae were dissected and cultured. Cells initially formed floating spheroids before transitioning to adherent monolayers. Cultures remained stable over several splits, whereas a marked reduction in cell number was observed at the eighth split due to the onset of contamination. Fluorescence microscopy confirmed nuclear integrity, while transmission electron microscopy at split 5 revealed cytoplasmic features consistent with insect fat body cells, including lipid droplets. The cell culture predominantly contained trophocyte-like cells, consistent with the known cellular composition of insect fat bodies. Transcriptomic analyses comparing fresh fat bodies and cultured cells revealed moderate transcriptional divergence, with limited upregulation of genes associated with iron homeostasis and stress response, consistent with adaptive responses to in vitro conditions. While not immortalized, this cell culture offers a short-term model for studying P. japonica physiology, toxicology, host–pathogen interactions, and potential gene-targeting strategies under controlled conditions. This work represents a first step toward enabling molecular and cellular research in this economically important pest species. Full article

Flammulina filiformis is the key industrial edible fungus that requires elevated CO₂ to promote the growth of long stipe and small pileus fruiting bodies. Heat shock transcription factors (HSFs) play vital roles in stress response and development regulation; yet the HSF gene family and its expression dynamics during fruiting body development in F. filiformis remain uncharacterized. This study aims to identify and characterize the HSF gene family in F. filiformis and to investigate their expression patterns during fruiting body development and in response to CO₂ treatments. In this study, 7 FfHSFs were identified, and their structures, sequence features, and phylogenetics were further analyzed. Expression patterns under CO₂ regulation were examined via qRT-PCR. The FfHSFs exhibited CDS lengths of 618–2298 bp, encoding 301–765 hydrophilic amino acids, with molecular weights ranging from 23.4 to 83.8 kDa and theoretical pI values between 4.75 and 9.15. All were predicted to be nuclear-localized. Cis-element analysis revealed motifs associated with growth regulation and stress responses such as low temperature, drought, and hypoxia. Phylogenetically, fungal HSFs were grouped into five clusters, with FfHSFs distributed across four. In this study, we examined the expression levels at four time points (0 h, 2 h, 12 h, and 36 h), under three different carbon dioxide concentrations (0.1%, 5%, and 20%) and in two types of tissues (pileus and stipe) for each six biological replicates. CO₂ treatments showed that 5% CO₂ significantly suppressed pileus expansion but not stipe elongation, while 20% CO₂ inhibited both. Under 20% CO₂ treatment, the pileus diameter decreased by approximately 40%, and simultaneously, the expression level of FfHSF1 decreased by about 70%. qRT-PCR indicated that FfHSF1 decreased with pileus expansion, whereas FfHSF4 increased. All FfHSFs were highly expressed in the stipe elongation zone. Elevated CO₂ down-regulated FfHSF1 in pileus and FfHSF6 in stipes. Based on these findings, it could be proposed that FfHSF1 and FfHSF6 might be candidate regulators in CO₂-mediated morphogenesis, providing insights into hormonal and environmental control of fruiting body development in F. filiformis. Full article

In vitro oocyte maturation (IVM) is a pivotal process influencing the success of embryo production in laboratory and clinical settings. However, oxidative stress (OS) often compromises oocyte quality during IVM. Antioxidants such as melatonin and epigallocatechin-3-gallate (EGCG) are known to mitigate OS by neutralizing reactive oxygen species (ROS) and bolstering antioxidant defenses. Despite extensive studies on their individual effects, the synergistic impact of melatonin and EGCG remains underexplored. Utilizing a mouse model, this study evaluated their combined effect on oocyte maturation, focusing on nuclear and cytoplasmic development, intracellular ROS, glutathione (GSH) levels, and subsequent embryonic competence. The results demonstrated that melatonin and EGCG significantly enhanced the polar body extrusion rate (p < 0.05), with the combination group achieving the highest rate of 91.96%. Cumulus expansion was observed to improve across all treated groups, with the combination treatment showing the highest cumulus expansion index (CEI) of 3.06. Furthermore, the combination treatment significantly reduced ROS levels and increased GSH content, indicating enhanced antioxidant capacity (p < 0.01). Embryonic development outcomes, including cleavage and blastocyst rates, were markedly higher in the combination group at 75.23% and 53.97%, respectively, demonstrating superior developmental potential (p < 0.01). These findings suggest that the melatonin–EGCG combination offers a novel and effective strategy to combat oxidative damage during IVM, thereby improving oocyte quality and embryonic development potential in mice. Full article

Plastic pollution is acknowledged as a serious problem for ecosystems. Among these plastics, polystyrene nanoplastics (PS-NPs) are emerging environmental pollutants, and their biological effects on hepatotoxicity are the least explored. Therefore, the present work examined the effect of PS-NPs on the hepatic transcription of the antioxidant genes Hmox1 and Sod3 in mice (n = 6, treatment (PS-NPs) vs. vehicle group (Veh)), mediated by RORγ and epigenetic modifications. The results show that PS-NP mice had significantly reduced body weight; increased activity of adenosine triphosphate (ATP), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH), and Complexes I, III, and V in the liver; and increased Alanine Transaminase (ALT), Aspartate Transaminase (ASP), Alkaline Phosphatase (ALP), malondialdehyde (MDA) and reactive oxygen species (ROS) compared to the Veh group. Furthermore, PS-NPs resulted in considerably lower relative mRNA expression of Hmox1, Sod3, and RORγ in the liver than the Veh group. Likewise, when compared to Veh, PS-NPs significantly reduced the enrichment of RORγ, as well as the occupancies of the key components of the transcriptional activation pathway (P300, SRC1, Pol II, Ser5-Pol II, and Ser2-Pol II) at the loci of Hmox1 and Sod3. In comparison to Veh, PS-NPs showed downregulated occupancies of the histone active marks H3K9ac and H3K18ac, while H3K4me3 and H3K27me3 were higher at the target loci of Hmox1 and Sod3. In conclusion, the present study highlights that PS-NPs induce oxidative stress by modifying Hmox1 and Sod3 in mice’s livers through histone changes and nuclear receptor RORγ modulation. Full article

Apiin, a natural flavonoid sourced from parsley, demonstrates antioxidant properties; however, its specific anti-aging effects have yet to be investigated in Caenorhabditis elegans (C. elegans). This research utilized C. elegans models to examine the anti-aging effects of apiin and the underlying mechanisms. The findings indicated that 100 μg/mL apiin extended the mean lifespan of C. elegans by 26.70%. Furthermore, apiin improved age-related characteristics in C. elegans, such as reducing intestine lipofuscin accumulation and increasing head thrashes and body bends. Additionally, apiin significantly improved stress resistance under thermal, ultraviolet, and oxidative stress conditions. Transcriptomic analysis revealed that apiin induced the differential expression of genes related to fatty acid metabolism, lipid catabolism, and oxidoreductase activity in C. elegans. Metabolomic data further corroborated the modulation of fatty acid metabolic processes by apiin. Biochemical assays, including lipid staining, triglyceride quantification, and measurements of antioxidant enzyme activity, demonstrated a decrease in lipid content and an enhancement in antioxidant capacity in C. elegans treated with apiin. Moreover, apiin promoted the nuclear translocation of DAF-16 and upregulated key longevity-associated genes, including sod-3, hsp-12.6, mtl-1, and ech-9. These results indicate that apiin mitigates aging in C. elegans through mechanisms involving the activation of DAF-16 and the regulation of lipid metabolism and oxidative stress responses. Our findings underscore the potential of apiin as a natural therapeutic agent for aging and associated metabolic disorders. Full article