The Protective Effect of Baicalin against UVB Irradiation Induced Photoaging: An In Vitro and In Vivo Study

Zhang, Mengli; Yin, Zhi; Ma, Li; Yin, Zhiqiang; Hu, Yawen; Xu, Yang; Wu, Di; Permatasari, Felicia; Luo, Dan; Zhou, Bingrong

doi:10.1371/journal.pone.0099703

Cited by 50 publications

(45 citation statements)

References 34 publications

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“…20,33 Baicalin is proved to be photoprotective to fibroblasts after UVB irradiation by the anti-photoaging effect. 34 It is also effective in inhibiting UVB-induced photodamage in keratinocytes by harvesting reactive oxygen species, 20 reducing the increased apoptosis rate and suppressing oxidative DNA adducts, in which process the relevant cytokine secretion and the expression of several genes like p53 and p21 were reduced. 35 Meanwhile, baicalin has been shown to induce autophagy in a variety of cell types including hepatocellular carcinoma cells, 26,36 breast cancer cells, 37 and even mice brain.…”

Section: Discussionmentioning

confidence: 99%

<p>Induction of Autophagy by Baicalin Through the AMPK-mTOR Pathway Protects Human Skin Fibroblasts from Ultraviolet B Radiation-Induced Apoptosis</p>

Zhang

Luan

Huang

et al. 2020

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These authors contributed equally to this work Background: Baicalin, a natural product isolated from Scutellaria radix, has been reported to exert anti-oxidant and anti-apoptotic effects on skin, but the underlying mechanism remains poorly understood. This study aimed to investigate the possible mechanism of anti-UVB effect of baicalin in human skin fibroblasts. Methods: Cell proliferation was estimated by CCK-8 Kit. Apoptotic incidence was detected by flow cytometry with Annexin V-PE/PI apoptosis detection kit. Autophagy was determined by the evaluation of fluorescent LC3 puncta and Western blotting. Cell signalling was analysed by Western blotting. Results: Baicalin exerted cytoprotective effects in UVB-induced HSFs. Moreover, baicalin increased autophagy and suppressed UVB-induced apoptosis of HSFs. Pretreatment with 3-MA, an autophagy inhibitor, attenuated baicalin-induced HSFs autophagy and promoted apoptosis. Baicalin activated AMPK, which leads to suppression of basal mTOR activity in cultured HSFs. Administration of compound C, an AMPK inhibitor, abrogated AMPK phosphorylation and increased mTOR phosphorylation and apoptosis compared with baicalin alone. Conclusion: Taken together, these results indicate the important role of mTOR inhibition in UVB protection by baicalin and provide a new target and strategy for better prevention of UV-induced skin disorders.

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Section: Discussionmentioning

confidence: 99%

<p>Induction of Autophagy by Baicalin Through the AMPK-mTOR Pathway Protects Human Skin Fibroblasts from Ultraviolet B Radiation-Induced Apoptosis</p>

Zhang

Luan

Huang

et al. 2020

DDDT

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“…This process can be triggered by both genetic (intrinsic ageing) and environmental (extrinsic ageing) factors. One of the most influential environmental factors is sun exposure, due mainly to ultraviolet (UV) irradiation, causing photodamage to the skin . UV irradiation‐induced photoageing arises mainly through the generation of severe oxidative stress in skin cells via interaction of UV with intracellular chromophores and photosensitizers.…”

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Chronic sun exposure is associated with distinct histone acetylation changes in human skin

et al. 2018

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“…Senescent cells are easily observed through β ‐galactosidase activity, which is why it is widely used to evaluate skin aging . This study is the first to describe HK activity protecting skin fibroblasts against CS‐dependent senescence, observed by reduction of β ‐galactosidase activity features in HFF‐1 culture.…”

Section: Discussionmentioning

confidence: 83%

Honokiol protects skin cells against inflammation, collagenolysis, apoptosis, and senescence caused by cigarette smoke damage

et al. 2017

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BACKGROUND Pollution, especially cigarette smoke, is a major cause of skin damage. OBJECTIVES To assess the effects of the small molecule polyphenol, honokiol, on reversing cigarette smoke induced damage in vitro to relevant skin cells. METHODS Keratinocytes (HaCat) cultures were exposed to cigarette smoke and, after 48 hours, IL-1α and IL-8 were measured in cell supernatants. Moreover, TIMP-2 production, apoptosis rate, and senescence β-galactosidase expression were evaluated in primary human fibroblasts (HFF-1) cultures. RESULTS Honokiol at 10 μM reduced IL-1α production by 3.4 folds (p<0.05), and at 10 and 20 μM reduced IL-8 by 23.9% and 53.1% (p<0.001), respectively, in HaCat keratinocytes. In HFF-1, honokiol restored TIMP-2 production by 96.9% and 91.9% (p<0.001), respectively, at 10 and 20 μM, as well as reduced apoptosis by 47.1% (p<0.001) and 41.3% (p<0.01), respectively. Finally, honokiol reduced senescence associated β-galactosidase expression in HFF-1. CONCLUSION Honokiol protects both HFF-1 and HaCat against cigarette smoke induced inflammation, collagenolysis, apoptosis, and senescence.

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The Protective Effect of Baicalin against UVB Irradiation Induced Photoaging: An In Vitro and In Vivo Study

Cited by 50 publications

References 34 publications

<p>Induction of Autophagy by Baicalin Through the AMPK-mTOR Pathway Protects Human Skin Fibroblasts from Ultraviolet B Radiation-Induced Apoptosis</p>

<p>Induction of Autophagy by Baicalin Through the AMPK-mTOR Pathway Protects Human Skin Fibroblasts from Ultraviolet B Radiation-Induced Apoptosis</p>

Chronic sun exposure is associated with distinct histone acetylation changes in human skin

Honokiol protects skin cells against inflammation, collagenolysis, apoptosis, and senescence caused by cigarette smoke damage

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