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金丝桃苷保护人原代黑素细胞免受H2O2诱导的氧化损伤。

Hyperoside protects human primary melanocytes against H2O2-induced oxidative damage.

作者信息

Yang Bin, Yang Qin, Yang Xin, Yan Hong-Bo, Lu Qi-Ping

机构信息

Department of Dermatology, Wuhan General Hospital of Guangzhou Command, Wuhan, Hubei 430070, P.R. China.

Department of Laboratory Medicine, Wuhan General Hospital of Guangzhou Command, Wuhan, Hubei 430070, P.R. China.

出版信息

Mol Med Rep. 2016 Jun;13(6):4613-9. doi: 10.3892/mmr.2016.5107. Epub 2016 Apr 12.

Abstract

Cuscutae semen has been shown to have beneficial effects in the treatment of vitiligo, recorded in the Chinese Pharmacopoeia, whereas the effects of its constituent compounds remains to be elucidated. Using a tetrazolium bromide assay, the present study found that hyperoside (0.5‑200 µg/ml) significantly increased the viability of human melanocytes in a time‑ and dose‑dependent manner. The present study used a cell model of hydrogen peroxide (H2O2)‑induced oxidative damage to examine the effect of hyperoside on human primary melanocytes. The results demonstrated that hyperoside pretreatment for 2 h decreased cell apoptosis from 54.03±9.11 to 17.46±3.10% in the H2O2‑injured melanocytes. The levels of oxidative stress in the mitochondrial membrane potential of the melanocytes increased following hyperoside pretreatment. The mRNA and protein levels of B‑cell lymphoma‑2/Bcl‑2‑associated X protein and caspase 3 were regulated by hyperoside, and phosphoinositide 3‑kinase/AKT and mitogen‑activated protein kinase signaling were also mediated by hyperoside. In conclusion, the results of the present study demonstrated that hyperoside protected the human primary melanocytes against oxidative damage.

摘要

菟丝子在《中国药典》中记载对白癜风治疗有有益作用,但其成分化合物的作用仍有待阐明。本研究采用溴化四氮唑蓝法,发现金丝桃苷(0.5-200μg/ml)能以时间和剂量依赖性方式显著提高人黑素细胞的活力。本研究使用过氧化氢(H2O2)诱导的氧化损伤细胞模型,研究金丝桃苷对人原代黑素细胞的影响。结果表明,在H2O2损伤的黑素细胞中,金丝桃苷预处理2小时可使细胞凋亡率从54.03±9.11%降至17.46±3.10%。金丝桃苷预处理后,黑素细胞线粒体膜电位的氧化应激水平升高。金丝桃苷可调节B细胞淋巴瘤-2/Bcl-2相关X蛋白和半胱天冬酶3的mRNA和蛋白水平,还可介导磷脂酰肌醇3激酶/AKT和丝裂原活化蛋白激酶信号传导。总之,本研究结果表明金丝桃苷可保护人原代黑素细胞免受氧化损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7a7/4878558/251ddccdc42c/MMR-13-06-4613-g00.jpg

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