Geniposide prevents H2O2-induced oxidative damage in melanocytes by activating the PI3K-Akt signalling pathway
Geniposide prevents H2O2-induced oxidative damage in melanocytes by activating the PI3K-Akt signalling pathway
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DOI：
10.1111/ced.13409
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发表时间：
2018-08-01
影响因子：
4.1
通讯作者：
Wang, K.
中科院分区：
文献类型：
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作者：
Lu, W.;Zhao, Y.;Wang, K.
氧化应激是白癜风的一种可能的致病因素，它可导致黑素细胞的破坏。京尼平苷通过激活磷酸肌醇3-激酶（PI 3 K）-Akt信号通路对多种细胞发挥一定的抗氧化作用。然而，研究人员还没有清楚地确定京尼平苷是否保护人类黑素细胞免受氧化应激或确定这种保护的潜在机制。目的确定京尼平苷是否保护黑素细胞免受H2 O2诱导的氧化损伤，并探讨PI 3 K-Akt信号通路在这种保护作用中的作用。活性氧（ROS）的产生和抗氧化酶超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的活性。我们研究了Akt，磷酸化Akt（p-Akt），Bcl-2，Bax，和裂解caspase 3和裂解caspase 9蛋白的表达，以确定参与的PI 3 K-Akt pathway.ResultsPretreatment与京尼平苷5，25，125或625 mol/L增加细胞活力和H2 O2处理的黑素细胞的凋亡率下降。京尼平苷还能增强SOD和CAT的抗氧化活性，降低细胞内ROS的积累。此外，京尼平苷增加P-Akt的水平，并调节PI 3 K-Akt通路中下游蛋白质的表达，如Bcl-2，Bax，以及切割的caspase 3和9，在H2 O2处理的黑素细胞中。值得注意的是，这些影响在很大程度上被阻断治疗LY 294002之前H2 O2 treatment.ConclusionsBased on这些结果，京尼平苷保护人类黑素细胞免受H2 O2诱导的氧化损伤，PI 3 K-Akt信号通路参与其抗氧化作用。
BackgroundOxidative stress is one possible pathogenic event in vitiligo that induces melanocyte destruction. Geniposide exerts certain antioxidant effects on various cells by activating the phosphoinositol 3-kinase (PI3K)-Akt signalling pathway. However, researchers have not clearly determined whether geniposide protects human melanocytes from oxidative stress or identified the underlying mechanism of such protection.AimTo determine whether geniposide protects melanocytes from H2O2-induced oxidative damage and to explore the role of the PI3K-Akt signalling pathway in this protective effect.MethodsThe antioxidant effects of geniposide on human melanocytes were examined by measuring cell viability, apoptosis rates, reactive oxygen species (ROS) production and activities of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT). We examined expression of Akt, phosphorylated Akt (p-Akt), Bcl-2, Bax, and cleaved caspase 3 and cleaved caspase 9 proteins to determine the involvement of the PI3K-Akt pathway.ResultsPretreatment with geniposide 5, 25, 125 or 625 mol/L increased cell viability and decreased the apoptosis rate of H2O2-treated melanocytes. In addition, geniposide enhanced the antioxidant activity of SOD and CAT, and decreased intracellular ROS accumulation. Furthermore, geniposide increased the levels of p-Akt and regulated the expression of downstream proteins in the PI3K-Akt pathway, such as Bcl-2, Bax, and cleaved caspase 3 and 9, in H2O2-treated melanocytes. Notably, these effects were largely blocked by treatment with LY294002 prior to H2O2 treatment.ConclusionsBased on these results, geniposide protects human melanocytes from H2O2-induced oxidative damage, and the PI3K-Akt signalling pathway is involved in its antioxidant effect.