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富含血小板的血浆可保护人类黑素细胞免受氧化应激,并改善 UVB 照射诱导的黑色素生成。

Platelet-rich plasma protects human melanocytes from oxidative stress and ameliorates melanogenesis induced by UVB irradiation.

机构信息

Guangdong Province Engineering Research Center for Antibody Drug and Immunoassay, College of Life Science and Technology, Jinan University, Guangzhou, Guangdong, China.

Department of Burn and Plastic Surgery, General Hospital of Southern Theater Command, PLA, Guangzhou, Guangdong, China.

出版信息

Biosci Biotechnol Biochem. 2021 Jun 24;85(7):1686-1696. doi: 10.1093/bbb/zbab085.

Abstract

To investigate the role of platelet-rich plasma (PRP) from different sources in alleviating oxidative stress and ameliorating melanogenesis in UVB-irradiated PIG1 cells, PIG1 cells were irradiated with 80 mJ/cm2 UVB prior to 1% PRP application and the following experiments were taken: the viability of UVB-irradiated PIG1 cells, cellular malondialdehyde (MDA) and reactive oxygen species (ROS) content, and activities of antioxidant enzymes. Western blotting was utilized to detect the expression level of proteins associated with melanin synthesis, apoptosis, and DNA lesions. We found that PRP intervention promoted cell proliferation, reduced MDA and ROS content, increased the activities of series of antioxidant enzymes, and alleviated DNA damages in UVB-damaged PIG1 cells. It is important to note that PRP treatment inhibited UVB-induced melanogenesis via the PI3K/Akt/GSK3β signal pathway. Therefore, we suppose PRP treatment exerts a protective role through their antioxidation effect on UVB-damaged PIG1 cells and hinders melanogenesis induced by UVB irradiation.

摘要

为了研究不同来源的富血小板血浆(PRP)在减轻 UVB 照射的 PIG1 细胞氧化应激和改善黑素生成中的作用,我们在 80 mJ/cm2 UVB 照射 PIG1 细胞之前应用了 1%的 PRP,并进行了以下实验:UVB 照射的 PIG1 细胞的活力、细胞丙二醛(MDA)和活性氧(ROS)含量以及抗氧化酶的活性。Western blot 用于检测与黑色素合成、细胞凋亡和 DNA 损伤相关的蛋白质表达水平。我们发现 PRP 干预促进了细胞增殖,降低了 MDA 和 ROS 含量,增加了一系列抗氧化酶的活性,并减轻了 UVB 损伤的 PIG1 细胞中的 DNA 损伤。值得注意的是,PRP 治疗通过 PI3K/Akt/GSK3β 信号通路抑制了 UVB 诱导的黑素生成。因此,我们推测 PRP 治疗通过其对 UVB 损伤的 PIG1 细胞的抗氧化作用发挥保护作用,并抑制 UVB 照射诱导的黑素生成。

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