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.

中文翻译：

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

为了研究不同来源的富含血小板的血浆 (PRP) 在减轻紫外线照射的 PIG1 细胞中的氧化应激和改善黑色素生成方面的作用，在应用 1% PRP 之前用 80 mJ/cm2 UVB 照射 PIG1 细胞，以下实验是采取：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。利用蛋白质印迹法检测与黑色素合成、细胞凋亡和 DNA 损伤相关的蛋白质的表达水平。我们发现PRP干预促进细胞增殖，降低MDA和ROS含量，增加一系列抗氧化酶的活性，减轻UVB损伤的PIG1细胞的DNA损伤。需要注意的是，PRP 处理通过 PI3K/Akt/GSK3β 信号通路抑制了 UVB 诱导的黑色素生成。因此，我们假设 PRP 处理通过其对 UVB 损伤的 PIG1 细胞的抗氧化作用发挥保护作用，并阻碍 UVB 照射诱导的黑色素生成。