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α-熊果苷通过调节SIRT3/PGC-1α通路改善UVA诱导的光老化。

α-Arbutin ameliorates UVA-induced photoaging through regulation of the SIRT3/PGC-1α pathway.

作者信息

Lu Fang, Zhou Qi, Liang Mengdi, Liang Huicong, Yu Yiwei, Li Yang, Zhang Yan, Lu Ling, Zheng Yan, Hao Jiejie, Shu Peng, Liu Jiankang

机构信息

Key Laboratory of Marine Drugs, Ministry of Education, School of Medicine and Pharmacy, Ocean University of China, Qingdao, China.

HBN Research Institute and Biological Laboratory, Shenzhen Hujia Technology Co., Ltd., Shenzhen, Guangdong, China.

出版信息

Front Pharmacol. 2024 Sep 23;15:1413530. doi: 10.3389/fphar.2024.1413530. eCollection 2024.

Abstract

Owing to its tyrosinase inhibitory activity, α-arbutin has been added to several skin care products as a skin-lightening agent. However, the protective effect of α-arbutin against ultraviolet A (UVA)-induced photoaging has not been well investigated. The present study was designed to investigate the photoprotective effect and mechanism of α-arbutin against UVA-induced photoaging. In vitro experiments, HaCaT cells were treated with UVA at a dose of 3 J/cm to evaluate the anti-photoaging effect of α-arbutin. α-Arbutin was found to exhibit a strong antioxidant effect by increasing glutathione (GSH) level and inhibiting reactive oxygen species (ROS) production. Meanwhile, α-arbutin markedly improved the expression of sirtuin 3 (SIRT3) and peroxisome proliferator-activated receptor γ coactivator 1 α (PGC-1α) proteins, initiating downstream signaling to increase mitochondrial membrane potential and mediate mitochondrial biogenesis, and improve mitochondrial structure significantly. In vivo analysis, the mice with shaved back hair were irradiated with a cumulative UVA dose of 10 J/cm and a cumulative ultraviolet B (UVB) dose of 0.63 J/cm. The animal experiments demonstrated that α-arbutin increased the expression of SIRT3 and PGC-1α proteins in the back skin of mice, thereby reducing UV-induced skin damage. In conclusion, α-arbutin protects HaCaT cells and mice from UVA damage by regulating SIRT3/PGC-1α signaling pathway.

摘要

由于其酪氨酸酶抑制活性,α-熊果苷已作为美白剂添加到多种护肤品中。然而,α-熊果苷对紫外线A(UVA)诱导的光老化的保护作用尚未得到充分研究。本研究旨在探讨α-熊果苷对UVA诱导的光老化的光保护作用及其机制。在体外实验中,用3 J/cm的UVA处理HaCaT细胞,以评估α-熊果苷的抗光老化作用。发现α-熊果苷通过提高谷胱甘肽(GSH)水平和抑制活性氧(ROS)生成而表现出强大的抗氧化作用。同时,α-熊果苷显著改善了沉默调节蛋白3(SIRT3)和过氧化物酶体增殖物激活受体γ共激活因子1α(PGC-1α)蛋白的表达,启动下游信号传导以增加线粒体膜电位并介导线粒体生物发生,并显著改善线粒体结构。在体内分析中,对背部毛发剃除的小鼠照射累积UVA剂量为10 J/cm和累积紫外线B(UVB)剂量为0.63 J/cm。动物实验表明,α-熊果苷增加了小鼠背部皮肤中SIRT3和PGC-1α蛋白的表达,从而减少了紫外线诱导的皮肤损伤。总之,α-熊果苷通过调节SIRT3/PGC-1α信号通路保护HaCaT细胞和小鼠免受UVA损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ab79/11456475/25791417b619/fphar-15-1413530-g001.jpg

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