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

Authors Zhang JA, Luan C, Huang D, Ju M, Chen K, Gu H

Received 22 August 2019

Accepted for publication 10 January 2020

Published 29 January 2020 Volume 2020:14 Pages 417—428

DOI https://doi.org/10.2147/DDDT.S228047

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Sukesh Voruganti


Jia-An Zhang,* Chao Luan,* Dan Huang, Mei Ju, Kun Chen, Heng Gu

Institute of Dermatology, Jiangsu Key Laboratory of Molecular Biology for Skin Diseases and STIs, Chinese Academy of Medical Science & Peking Union Medical College, Nanjing, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Kun Chen; Heng Gu
Institute of Dermatology, Jiangsu Key Laboratory of Molecular Biology for Skin Diseases and STIs, Chinese Academy of Medical Science & Peking Union Medical College, 12 JiangWangMiao Street, Nanjing, Jiangsu 210029, People’s Republic of China
Tel/Fax +86 25 85478030
Email kunchen181@aliyun.com; doctor_guheng@hotmail.com

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.

Keywords: autophagy, baicalin, ultraviolet B, apoptosis, AMPK

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