Department of Dermatology, Qilu Hospital of Shandong University (Qingdao), Qingdao, China.
Department of Dermatology, Qilu Hospital of Shandong University, Jinan, China.
Clin Exp Dermatol. 2018 Aug;43(6):667-674. doi: 10.1111/ced.13409. Epub 2018 Mar 7.
Oxidative 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.
To determine whether geniposide protects melanocytes from H O -induced oxidative damage and to explore the role of the PI3K-Akt signalling pathway in this protective effect.
The 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.
Pretreatment with geniposide 5, 25, 125 or 625 μmol/L increased cell viability and decreased the apoptosis rate of H O -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 H O -treated melanocytes. Notably, these effects were largely blocked by treatment with LY294002 prior to H O treatment.
Based on these results, geniposide protects human melanocytes from H O -induced oxidative damage, and the PI3K-Akt signalling pathway is involved in its antioxidant effect.
氧化应激是导致黑色素细胞破坏的白癜风发病的一个可能的病理事件。栀子苷通过激活磷脂酰肌醇 3-激酶（PI3K）-Akt 信号通路对各种细胞发挥一定的抗氧化作用。然而，研究人员尚未明确确定栀子苷是否能保护人黑色素细胞免受氧化应激的影响，也未确定这种保护作用的潜在机制。
确定栀子苷是否能保护黑色素细胞免受 H 2 O 2 诱导的氧化损伤，并探讨 PI3K-Akt 信号通路在这种保护作用中的作用。
通过测量细胞活力、凋亡率、活性氧（ROS）产生和抗氧化酶超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的活性来研究栀子苷对人黑色素细胞的抗氧化作用。我们检测了 Akt、磷酸化 Akt（p-Akt）、Bcl-2、Bax 和裂解的 caspase 3 和 9 蛋白的表达，以确定 PI3K-Akt 通路的参与情况。
用 5、25、125 或 625 μmol/L 的栀子苷预处理可增加 H 2 O 2 处理的黑色素细胞的活力并降低其凋亡率。此外，栀子苷增强了 SOD 和 CAT 的抗氧化活性，减少了细胞内 ROS 的积累。此外，栀子苷增加了 PI3K-Akt 通路下游蛋白如 Bcl-2、Bax 和裂解的 caspase 3 和 9 的表达，同时上调了 H 2 O 2 处理的黑色素细胞中的 p-Akt 水平。值得注意的是，这些作用在先用 LY294002 预处理 H 2 O 2 处理之前，大部分被阻断。
基于这些结果，栀子苷可保护人黑色素细胞免受 H 2 O 2 诱导的氧化损伤，PI3K-Akt 信号通路参与其抗氧化作用。
