Anticatabolic and Anti-Inflammatory Effects of Myricetin 3-O-β-d-Galactopyranoside in UVA-Irradiated Dermal Cells via Repression of MAPK/AP-1 and Activation of TGFβ/Smad

Oh, Jung Hwan; Karadeniz, Fatih; Lee, Jung Im; Park, So Young; Seo, Youngwan; Kong, Chang‐Suk

doi:10.3390/molecules25061331

Cited by 23 publications

(16 citation statements)

References 36 publications

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“…Cell viability was above 90% up to 10 µM, which was chosen as the highest dose of treatment. UVA irradiation was carried out at 10 J/cm 2 dose which was previously reported to be non-toxic for 24 h while inducing photoaging mechanisms (MMP-1 activation and inhibition of collagen synthesis) in HDFs [23]. Ahn et al [22] reported that (2′S)-columbianetin showed a significant scavenging effect against UVB-mediated reactive oxygen species (ROS) generation in keratinocytes.…”

Section: Resultsmentioning

confidence: 99%

Antiphotoaging Effect of (2′S)-Columbianetin from Corydalis heterocarpa in UVA-Irradiated Human Dermal Fibroblasts

Karadeniz

Lee

et al. 2020

Applied Sciences

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Ultraviolet A (UVA)-induced detrimental effects in the skin, also known as photoaging, are mediated with several pathways including oxidative stress generation and extracellular matrix (ECM) degradation. UVA irradiation results in excessive production of matrix metalloproteinases (MMPs), enzymes responsible for the degradation of ECM components such as collagen. In this study, the protective effects of (2 S)-columbianetin against UVA-induced changes in matrix metalloproteinase-1 (MMP-1) and collagen production were investigated in human dermal fibroblasts (HDFs). The (2 S)-columbianetin was isolated from Corydalis heterocarpa. UVA exposure increased MMP-1 release from HDFs and diminished the release of type I pro-collagen. Treatment with (2 S)-columbianetin reversed these effects of UVA exposure. The (2 S)-columbianetin treatment also suppressed the intracellular expression of MMP-1 and increased type I pro-collagen expression. UVA exposure elevated the activation of p38, c-Jun-amino-terminal kinase (JNK) and extracellular signal-related kinase (ERK) as the mechanism to stimulate MMP-1 production. The (2 S)-columbianetin suppressed the phosphorylation of JNK and ERK. The (2 S)-columbianetin was also stimulated collagen production via TGFβ signaling cascade, relieving UVA-induced suppression of Smad2/3 phosphorylation and translocation. In conclusion, (2 S)-columbianetin was suggested to be a potential cosmeceutical lead compound with antiphotoaging properties against UVA-induced collagen degradation.

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Section: Resultsmentioning

confidence: 99%

Antiphotoaging Effect of (2′S)-Columbianetin from Corydalis heterocarpa in UVA-Irradiated Human Dermal Fibroblasts

Karadeniz

Lee

et al. 2020

Applied Sciences

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“…While IL-6, TNF-α, and IL-1β are involved in mediating inflammatory responses, IL-10 and TGF-β1 are well known anti-inflammatory cytokines that inhibit the secretion of pro-inflammatory cytokines and attenuate inflammation [ 30 , 31 ]. In our study, stevioside was demonstrated to be capable of enhancing IL-10 and TGF-β1 expression to some extent in LPS-treated macrophages from the three sources and in LPS-treated mice as well.…”

Section: Discussionmentioning

confidence: 99%

Stevioside Activates AMPK to Suppress Inflammation in Macrophages and Protects Mice from LPS-Induced Lethal Shock

Wei

Zhu

et al. 2021

Molecules

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Stevioside, a diterpenoid glycoside, is widely used as a natural sweetener; meanwhile, it has been proven to possess various pharmacological properties as well. However, until now there were no comprehensive evaluations focused on the anti-inflammatory activity of stevioside. Thus, the anti-inflammatory activities of stevioside, both in macrophages (RAW 264.7 cells, THP-1 cells, and mouse peritoneal macrophages) and in mice, were extensively investigated for the potential application of stevioside as a novel anti-inflammatory agent. The results showed that stevioside was capable of down-regulating lipopolysaccharide (LPS)-induced expression and production of pro-inflammatory cytokines and mediators in macrophages from different sources, such as IL-6, TNF-α, IL-1β, iNOS/NO, COX2, and HMGB1, whereas it up-regulated the anti-inflammatory cytokines IL-10 and TGF-β1. Further investigation showed that stevioside could activate the AMPK -mediated inhibition of IRF5 and NF-κB pathways. Similarly, in mice with LPS-induced lethal shock, stevioside inhibited release of pro-inflammatory factors, enhanced production of IL-10, and increased the survival rate of mice. More importantly, stevioside was also shown to activate AMPK in the periphery blood mononuclear cells of mice. Together, these results indicated that stevioside could significantly attenuate LPS-induced inflammatory responses both in vitro and in vivo through regulating several signaling pathways. These findings further strengthened the evidence that stevioside may be developed into a therapeutic agent against inflammatory diseases.

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“…MAPK signaling cascade plays a pivotal role in MMP gene expression [ 26 , 27 ]. Overexposure to UV radiation can trigger the activation of MAPK pathway and its subfamilies, the p38, JNK and ERK proteins, leading to stimulation of the translocation of AP-1 [ 28 , 29 , 30 ]. The MAPK-inducible transcriptional complex AP-1, which consists of c-Fos and c-Jun proteins, translocates into the nucleus, where it induces the activation of MMP promoters.…”

Section: Discussionmentioning

confidence: 99%

“…The HDFs were harvested and washed three times by PBS. Total cellular protein was extracted and investigated, using immunoblotting, as previous published [ 29 ]. The nuclear fraction was extracted by NE-PER TM Nuclear and cytoplasmic extraction reagents kit (Catalog No.…”

Section: Methodsmentioning

confidence: 99%

Antiphotoaging Effect of 3,5-Dicaffeoyl-epi-quinic Acid against UVA-Induced Skin Damage by Protecting Human Dermal Fibroblasts In Vitro

Karadeniz

Kong

et al. 2020

IJMS

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Cutaneous aging is divided into intrinsic and exogenous aging correspondingly contributing to the complex biological phenomenon in skin. Intrinsic aging is also termed chronological aging, which is the accumulation of inevitable changes over time and is largely genetically determined. Superimposed on this intrinsic process, exogenous aging is associated with environmental exposure, mainly to ultraviolet (UV) radiation and more commonly termed as photoaging. UV-induced skin aging induces increased expression of matrix metalloproteinases (MMPs) which in turn causes the collagen degradation. Therefore, MMP inhibitors of natural origin are regarded as a primary approach to prevent or treat photoaging. This study investigated the effects of 3,5-dicaffeoyl-epi-quinic acid (DEQA) on photoaging and elucidated its molecular mechanisms in UVA-irradiated human dermal fibroblasts (HDFs). The results show that treatment with DEQA decreases MMP-1 production and increases type I collagen production in UVA-damaged HDFs. In addition, treatment of UVA-irradiated HDFs with DEQA downregulates MMP-1, MMP-3 and MMP-9 expression via blocking MAPK-cascade-regulated AP-1 transcriptional activity in UVA-irradiated HDFs. Furthermore, DEQA relieves the UVA-mediated suppression of type I procollagen and collagen expression through stimulating TGF-β/Smad signaling, leading to activation of the Smad 2/3 and Smad 4 nuclear translocation. These results suggest that DEQA could be a potential cosmetic agent for prevention and treatment of skin photoaging.

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Anticatabolic and Anti-Inflammatory Effects of Myricetin 3-O-β-d-Galactopyranoside in UVA-Irradiated Dermal Cells via Repression of MAPK/AP-1 and Activation of TGFβ/Smad

Cited by 23 publications

References 36 publications

Antiphotoaging Effect of (2′S)-Columbianetin from Corydalis heterocarpa in UVA-Irradiated Human Dermal Fibroblasts

Antiphotoaging Effect of (2′S)-Columbianetin from Corydalis heterocarpa in UVA-Irradiated Human Dermal Fibroblasts

Stevioside Activates AMPK to Suppress Inflammation in Macrophages and Protects Mice from LPS-Induced Lethal Shock

Antiphotoaging Effect of 3,5-Dicaffeoyl-epi-quinic Acid against UVA-Induced Skin Damage by Protecting Human Dermal Fibroblasts In Vitro

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