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Biological Interactions of Bioactive Natural Products

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Bioactives and Nutraceuticals".

Deadline for manuscript submissions: closed (28 February 2022) | Viewed by 32566

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Prof. Dr. Seung-Hong Lee

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Guest Editor

Department of Pharmaceutical Engineering, Soonchunhyang University, Asan, Korea
Interests: natural products nutraceuticals; cosmeceuticals; pharmaceuticals; bioactive compounds; marine organisms; phytomedicine
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Ginnae Ahn

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Guest Editor

Department of Marine Bio Food Science, College of Fisheries and Ocean Science, Chonnam National University, Gwangju, Korea
Interests: functional food; food bioactives; bioactive compounds; marine nutraceuticals
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Bioactive natural products are secondary metabolites of plants and animals generated through various biological pathways. The bioactive natural products have a wide range of possible applications, such as biomedicine and pharmacotherapy, which can be useful in treatment and management various kinds of human diseases due to their outstanding biological properties. This Special Issue will shape the future research direction of important bioactive natural products, as well as related bioactives. Our purpose is to feature high-quality, advanced research and knowledge contributed by various research groups working on bioactive natural products from all around the world. This Special Issue covers recent innovations relating to various bioactive natural products and their applications in the pharmaceutical, nutraceutical, and cosmeceutical fields related to academia, research, and industry. This Special Issue’s emphasis is placed on biological mechanisms associated with interactions between bioactive natural products and biological systems. Outcomes may include all traditional endpoints caused by naturally occurring chemicals, both in vivo and in vitro. Endpoints of interest include but are not limited to preventing and managing human diseases, human health and skin aging, new strategies of using natural drugs, and biotechnology for yielding bioactives.

Prof. Dr. Seung-Hong Lee
Prof. Dr. Ginnae Ahn
Guest Editors

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Keywords

Bioactive natural products
Biomedicine
Pharmacotherapy
Mechanism of action
Human health and diseases
Skin aging

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Published Papers (9 papers)

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Research

22 pages, 4078 KiB

Open AccessArticle

Dendrobium nobile Lindley Administration Attenuates Atopic Dermatitis-like Lesions by Modulating Immune Cells

by Sooyeon Hong, Eun-Young Kim, Seo-Eun Lim, Jae-Hyun Kim, Youngjoo Sohn and Hyuk-Sang Jung

Int. J. Mol. Sci. 2022, 23(8), 4470; https://doi.org/10.3390/ijms23084470 - 18 Apr 2022

Cited by 19 | Viewed by 3564

Abstract

Atopic dermatitis (AD) is a chronic inflammatory skin disease that can significantly affect daily life by causing sleep disturbance due to extreme itching. In addition, if the symptoms of AD are severe, it can cause mental disorders such as ADHD and suicidal ideation. Corticosteroid preparations used for general treatment have good effects, but their use is limited due to side effects. Therefore, it is essential to minimize the side effects and study effective treatment methods. Dendrobium nobile Lindley (DNL) has been widely used for various diseases, but to the best of our knowledge, its effect on AD has not yet been proven. In this study, the inhibitory effect of DNL on AD was confirmed in a DNCB-induced Balb/c mouse. In addition, the inhibitory efficacy of inflammatory cytokines in TNF-α/IFN-γ-induced HaCaT cells and PMACI-induced HMC-1 cells was confirmed. The results demonstrated that DNL decreased IgE, IL-6, IL-4, scratching behavior, SCORAD index, infiltration of mast cells and eosinophils and decreased the thickness of the skin. Additionally, DNL inhibited the expression of cytokines and inhibited the MAPK and NF-κB signaling pathways. This suggests that DNL inhibits cytokine expression, protein signaling pathway, and immune cells, thereby improving AD symptoms in mice. Full article

(This article belongs to the Special Issue Biological Interactions of Bioactive Natural Products)

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15 pages, 3907 KiB

Open AccessArticle

Indigo Pulverata Levis (Chung-Dae, Persicaria tinctoria) Alleviates Atopic Dermatitis-like Inflammatory Responses In Vivo and In Vitro

by Ga-Yul Min, Ji-Hye Kim, Tae-In Kim, Won-Kyung Cho, Ju-Hye Yang and Jin-Yeul Ma

Int. J. Mol. Sci. 2022, 23(1), 553; https://doi.org/10.3390/ijms23010553 - 5 Jan 2022

Cited by 9 | Viewed by 3650

Abstract

Atopic dermatitis (AD) is a chronic inflammatory skin disease associated with a type 2 T helper cell (Th2) immune response. The IndigoPulverata Levis extract (CHD) is used in traditional Southeast Asian medicine; however, its beneficial effects on AD remain uninvestigated. Therefore, we investigated the therapeutic effects of CHD in 2,4-dinitrochlorobenzene (DNCB)-induced BALB/c mice and tumor necrosis factor (TNF)-α- and interferon gamma (IFN)-γ-stimulated HaCaT cells. We evaluated immune cell infiltration, skin thickness, and the serum IgE and TNF-α levels in DNCB-induced AD mice. Moreover, we measured the expression levels of pro-inflammatory cytokines, mitogen-activated protein kinase (MAPK), and the nuclear factor-kappa B (NF-κB) in the mice dorsal skin. We also studied the effect of CHD on the translocation of NF-κB p65 and inflammatory chemokines in HaCaT cells. Our in vivo results revealed that CHD reduced the dermis and epidermis thicknesses and inhibited immune cell infiltration. Furthermore, it suppressed the proinflammatory cytokine expression and MAPK and NF-κB phosphorylations in the skin tissue and decreased serum IgE and TNF-α levels. In vitro results indicated that CHD downregulated inflammatory chemokines and blocked NF-κB p65 translocation. Thus, we deduced that CHD is a potential drug candidate for AD treatment. Full article

(This article belongs to the Special Issue Biological Interactions of Bioactive Natural Products)

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17 pages, 3812 KiB

Open AccessArticle

Honokiol Acts as a Potent Anti-Fibrotic Agent in the Liver through Inhibition of TGF-β1/SMAD Signaling and Autophagy in Hepatic Stellate Cells

by Seita Kataoka, Atsushi Umemura, Keiichiro Okuda, Hiroyoshi Taketani, Yuya Seko, Taichiro Nishikawa, Kanji Yamaguchi, Michihisa Moriguchi, Yoshihiro Kanbara, Jack L. Arbiser, Toshihide Shima, Takeshi Okanoue and Yoshito Itoh

Int. J. Mol. Sci. 2021, 22(24), 13354; https://doi.org/10.3390/ijms222413354 - 12 Dec 2021

Cited by 16 | Viewed by 3637

Abstract

Chronic liver injury may result in hepatic fibrosis, which can progress to cirrhosis and eventually liver failure. There are no drugs that are specifically approved for treating hepatic fibrosis. The natural product honokiol (HNK), a bioactive compound extracted from Magnolia grandiflora, represents a potential tool in the management of hepatic fibrosis. Though HNK has been reported to exhibit suppressive effects in a rat fibrosis model, the mechanisms accounting for this suppression remain unclear. In the present study, the anti-fibrotic effects of HNK on the liver were evaluated in vivo and in vitro. In vivo studies utilized a murine liver fibrosis model, in which fibrosis is induced by treatment with carbon tetrachloride (CCl₄). For in vitro studies, LX-2 human hepatic stellate cells (HSCs) were treated with HNK, and expression of markers of fibrosis, cell viability, the transforming growth factor-β (TGF-β1)/SMAD signaling pathway, and autophagy were analyzed. HNK was well tolerated and significantly attenuated CCl₄-induced liver fibrosis in vivo. Moreover, HNK decreased HSC activation and collagen expression by downregulating the TGF-β1/SMAD signaling pathway and autophagy. These results suggest that HNK is a new potential candidate for the treatment of hepatic fibrosis through suppressing both TGF-β1/SMAD signaling and autophagy in HSCs. Full article

(This article belongs to the Special Issue Biological Interactions of Bioactive Natural Products)

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15 pages, 2856 KiB

Open AccessArticle

Olfactory Receptor OR7A17 Expression Correlates with All-Trans Retinoic Acid (ATRA)-Induced Suppression of Proliferation in Human Keratinocyte Cells

by Hyeyoun Kim, See-Hyoung Park, Sae Woong Oh, Kitae Kwon, Se Jung Park, Eunbi Yu, Seyoung Yang, Jung Yoen Park, Seoyoung Choi, Seoyoun Yang, Su Bin Han, Minkyung Song, Jae Youl Cho and Jongsung Lee

Int. J. Mol. Sci. 2021, 22(22), 12304; https://doi.org/10.3390/ijms222212304 - 14 Nov 2021

Cited by 8 | Viewed by 3086

Abstract

Olfactory receptors (ORs), which belong to the G-protein-coupled receptor family, have been widely studied as ectopically expressed receptors in various human tissues, including the skin. However, the physiological functions of only a few OR types have been elucidated in skin cells. All-trans retinoic acid (ATRA) is a well-known medication for various skin diseases. However, many studies have shown that ATRA can have adverse effects, resulting from the suppression of cell proliferation. Here, we investigated the involvement of OR7A17 in the ATRA-induced suppression of human keratinocyte (HaCaT) proliferation. We demonstrated that OR7A17 is expressed in HaCaT keratinocytes, and its expression was downregulated by ATRA. The ATRA-induced downregulation of OR7A17 was attenuated via RAR α or RAR γ antagonist treatment, indicating that the effects of ATRA on OR7A17 expression were mediated through nuclear retinoic acid receptor signaling. Moreover, we found that the overexpression of OR7A17 induced the proliferation of HaCaT cells while counteracting the antiproliferative effect of ATRA. Mechanistically, OR7A17 overexpression reversed the ATRA-induced attenuation of Ca²⁺ entry. Our findings indicated that ATRA suppresses cell proliferation through the downregulation of OR7A17 via RAR α- and γ-mediated retinoid signaling. Taken together, OR7A17 is a potential therapeutic target for ameliorating the anti-proliferative effects of ATRA. Full article

(This article belongs to the Special Issue Biological Interactions of Bioactive Natural Products)

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10 pages, 1760 KiB

Open AccessArticle

Primary Ciliogenesis by 2-Isopropylmalic Acid Prevents PM2.5-Induced Inflammatory Response and MMP-1 Activation in Human Dermal Fibroblasts and a 3-D-Skin Model

by Ji-Eun Bae, Daejin Min, Ji Yeon Choi, Hyunjung Choi, Joon Bum Kim, Na Yeon Park, Doo Sin Jo, Yong Hwan Kim, Hye-Won Na, Yoon Jae Kim, Eun Sung Kim, Hyoung-June Kim and Dong-Hyung Cho

Int. J. Mol. Sci. 2021, 22(20), 10941; https://doi.org/10.3390/ijms222010941 - 10 Oct 2021

Cited by 7 | Viewed by 2836

Abstract

Particulate matters (PMs) increase oxidative stress and inflammatory response in different tissues. PMs disrupt the formation of primary cilia in various skin cells, including keratinocytes and melanocytes. In this study, we found that 2-isopropylmalic acid (2-IPMA) promoted primary ciliogenesis and restored the PM2.5-induced dysgenesis of primary cilia in dermal fibroblasts. Moreover, 2-IPMA inhibited the generation of excessive reactive oxygen species and the activation of stress kinase in PM2.5-treated dermal fibroblasts. Further, 2-IPMA inhibited the production of pro-inflammatory cytokines, including IL-6 and TNF-α, which were upregulated by PM2.5. However, the inhibition of primary ciliogenesis by IFT88 depletion reversed the downregulated cytokines by 2-IPMA. Moreover, we found that PM2.5 treatment increased the MMP-1 expression in dermal fibroblasts and a human 3-D-skin model. The reduced MMP-1 expression by 2-IPMA was further reversed by IFT88 depletion in PM2.5-treated dermal fibroblasts. These findings suggest that 2-IPMA ameliorates PM2.5-induced inflammation by promoting primary ciliogenesis in dermal fibroblasts. Full article

(This article belongs to the Special Issue Biological Interactions of Bioactive Natural Products)

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11 pages, 3458 KiB

Open AccessArticle

Weak Interactions of the Isomers of Phototrexate and Two Cavitand Derivatives

by Zsolt Preisz, Zoltán Nagymihály, László Kollár, Tamás Kálai and Sándor Kunsági-Máté

Int. J. Mol. Sci. 2021, 22(19), 10764; https://doi.org/10.3390/ijms221910764 - 5 Oct 2021

Cited by 3 | Viewed by 2036

Abstract

The interactions of two conformers of newly synthesized photoswitchable azobenzene analogue of methotrexate, called Phototrexate, with two cavitand derivatives, have been investigated in dimethyl sulfoxide medium. Photoluminescence methods have been applied to determine the complex stabilities and the related enthalpy and entropy changes associated to the complex formation around room temperature. Results show opposite temperature dependence of complex stabilities. The structure of the upper rims of the host molecules and the reordered solvent structure were identified as the background of the opposite tendencies of temperature dependence at molecular level. These results can support the therapeutic application of the photoswitchable phototrexate, because the formation of inclusion complexes is a promising method to regulate the pharmacokinetics of drug molecules. Full article

(This article belongs to the Special Issue Biological Interactions of Bioactive Natural Products)

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15 pages, 9156 KiB

Open AccessArticle

Anti-Inflammatory Effects of Metabolites from Antarctic Fungal Strain Pleosporales sp. SF-7343 in HaCaT Human Keratinocytes

by Linsha Dong, Hye Jin Kim, Thao Quyen Cao, Zhiming Liu, Hwan Lee, Wonmin Ko, Youn-Chul Kim, Jae Hak Sohn, Tai Kyoung Kim, Joung Han Yim, Dong-Sung Lee and Hyuncheol Oh

Int. J. Mol. Sci. 2021, 22(18), 9674; https://doi.org/10.3390/ijms22189674 - 7 Sep 2021

Cited by 13 | Viewed by 3327

Abstract

Chemical investigation of the Antarctic fungi Pleosporales sp. SF-7343 revealed four known secondary fungal metabolites: alternate C (1), altenusin (2), alternariol (3), and altenuene (4). The compound structures were identified primarily by NMR and MS analyses. Atopic dermatitis, an inflammatory disease, is driven by the abnormal activation of T helper (Th) 2 cells and barrier dysfunction. We attempted to identify the anti-inflammatory components of SF-7343. Initial screening showed that compounds 1 and 3 inhibited the secretion of interleukin-8 and -6 in tumor necrosis factor-α/interferon-γ-treated HaCaT cells, and these compounds also showed inhibitory effects on CCL5 and CCL22. Compounds 1 and 3 also downregulated the protein expression levels of intercellular adhesion molecule-1 and upregulated the expression of filaggrin and involcurin. The mechanism study results showed that compounds 1 and 3 inhibited nuclear translocation of nuclear factor-kappa B p65 and the phosphorylation of STAT1 and STAT3. Compound 1, but not compound 3, significantly promoted the expression of heme oxygenase (HO)-1. The effects of compound 1 were partly reversed by co-treatment with a HO-1 inhibitor, tin protoporphyrin IX. Taken together, this study demonstrates the potential value of Antarctic fungal strain SF-7343 isolates as a bioresource for bioactive compounds to prevent skin inflammation. Full article

(This article belongs to the Special Issue Biological Interactions of Bioactive Natural Products)

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20 pages, 5859 KiB

Open AccessArticle

Dietary Collagen Hydrolysates Ameliorate Furrowed and Parched Skin Caused by Photoaging in Hairless Mice

by Min-Kyung Kang, Dong-Yeon Kim, Hyeongjoo Oh, Soo-Il Kim, Su-Yeon Oh, Woojin Na, Sin-Hye Park, Kyungho Park, Jun-Il Kim, Ae-Hyang Kim and Young-Hee Kang

Int. J. Mol. Sci. 2021, 22(11), 6137; https://doi.org/10.3390/ijms22116137 - 7 Jun 2021

Cited by 18 | Viewed by 5384

Abstract

Collagen hydrolysates have been suggested as a favorable antiaging modality in skin photoaged by persistent exposure to ultraviolet radiation (UV). The current study evaluated the beneficial effect of collagen hydrolysates (fsCH) extracted from Pangasius hypophthalmus fish skin on wrinkle formation and moisture preservation in dorsal skin of hairless mice challenged with UV-B. Inter-comparative experiments were conducted for anti-photoaging among fsCH, retinoic acid (RA), N-acetyl-D-glucosamine (NAG), and glycine-proline-hydroxyproline (GPH). Treating human HaCaT keratinocytes with 100−200 μg/mL fsCH reciprocally ameliorated the expression of aquaporin 3 (AQP3) and CD44 deranged by UV-B. The UV-B-induced deep furrows and skin thickening were improved in parched dorsal skin of mice supplemented with 206–412 mg/kg fsCH as well as RA and GPH. The UV-B irradiation enhanced collagen fiber loss in the dorsal dermis, which was attenuated by fsCH through enhancing procollagen conversion to collagen. The matrix metalloproteinase expression by UV-B in dorsal skin was diminished by fsCH, similar to RA and GPH, via blockade of collagen degradation. Supplementing fsCH to UV-B-irradiated mice decreased transepidermal water loss in dorsal skin with reduced AQP3 level and restored keratinocyte expression of filaggrin. The expression of hyaluronic acid synthase 2 and hyaluronidase 1 by UV-B was remarkably ameliorated with increased production of hyaluronic acid by treating fsCH to photoaged mice. Taken together, fsCH attenuated photoaging typical of deep wrinkles, epidermal thickening, and skin water loss, like NAG, RA, or GPH, through inhibiting collagen destruction and epidermal barrier impairment. Full article

(This article belongs to the Special Issue Biological Interactions of Bioactive Natural Products)

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18 pages, 19660 KiB

Open AccessArticle

Ganoderic Acid A Promotes Amyloid-β Clearance (In Vitro) and Ameliorates Cognitive Deficiency in Alzheimer’s Disease (Mouse Model) through Autophagy Induced by Activating Axl

by Li-Feng-Rong Qi, Shuai Liu, Yu-Ci Liu, Ping Li and Xiaojun Xu

Int. J. Mol. Sci. 2021, 22(11), 5559; https://doi.org/10.3390/ijms22115559 - 24 May 2021

Cited by 31 | Viewed by 3728

Abstract

Alzheimer’s disease (AD) is thought to be caused by amyloid-β (Aβ) accumulation in the central nervous system due to deficient clearance. The aim of the present study was to investigate the effect of ganoderic acid A (GAA) on Aβ clearance in microglia and its anti-AD activity. Aβ degradation in BV2 microglial cells was determined using an intracellular Aβ clearance assay. GAA stimulated autophagosome formation via the Axl receptor tyrosine kinase (Axl)/RAC/CDC42-activated kinase 1 (Pak1) pathway was determined by Western blot analyses, and fluorescence-labeled Aβ42 was localized in lysosomes in confocal laser microscopy images. The in vivo anti-AD activity of GAA was evaluated by object recognition and Morris water maze (MWM) tests in an AD mouse model following intracerebroventricular injection of aggregated Aβ42. The autophagy level in the hippocampus was assayed by immunohistochemical assessment against microtubule-associated proteins 1A/1B light-chain 3B (LC3B). Intracellular Aβ42 levels were significantly reduced by GAA treatment in microglial cells. Additionally, GAA activated autophagy according to increased LC3B-II levels, with this increased autophagy stimulated by upregulating Axl and Pak1 phosphorylation. The effect of eliminating Aβ by GAA through autophagy was reversed by R428, an Axl inhibitor, or IPA-3, a Pak1 inhibitor. Consistent with the cell-based assay, GAA ameliorated cognitive deficiency and reduced Aβ42 levels in an AD mouse model. Furthermore, LC3B expression in the hippocampus was up-regulated by GAA treatment, with these GAA-specific effects abolished by R428. GAA promoted Aβ clearance by enhancing autophagy via the Axl/Pak1 signaling pathway in microglial cells and ameliorated cognitive deficiency in an AD mouse model. Full article

(This article belongs to the Special Issue Biological Interactions of Bioactive Natural Products)

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