青蒿素通过Nrf2/HO-1通路改善Aβ_(1-42)对SH-SY5Y细胞的细胞毒性作用

Artemisinin attenuates the cytotoxicity induced by Aβ_(1-42) in SH-SY5Y cells through Nrf2/HO-1 pathway

目的研究青蒿素(Artemisinin)在β淀粉样蛋白1-42(amyloid-β1-42,Aβ1-42)诱导的SH-SY5Y细胞毒性作用中的保护性作用及其可能机制。方法 SH-SY5Y细胞分为control组、Aβ1-42组、control+Aβ1-42组和Artemisinin+Aβ1-42组。利用细胞增殖实验检测细胞增殖情况,乳酸脱氢酶细胞毒性检测实验检测细胞的受损情况,免疫荧光检测细胞内活性氧(reactive oxygen species,ROS)的表达水平,Western blotting检测Nrf2和HO-1蛋白的表达。结果与control组相比,Artemisinin能够改善Aβ1-42对SH-SY5Y细胞的损伤以及增殖活力的抑制。除此之外,Artemisinin还能够抑制Aβ1-42诱导的SH-SY5Y细胞内ROS的表达,上调Nrf2和HO-1蛋白的表达。结论 Artemisinin能够通过Nrf2/HO-1通路改善Aβ1-42诱导的氧化应激对SH-SY5Y细胞的毒性作用。

Objective To study the protective effect of Artemisinin on the cytotoxicity induced by Aβ 1-42 in SH-SY5Y cells and its possible mechanism. Methods SH-SY5Y cells were divided into control group,Aβ 1-42 group,control ＋ Aβ 1-42 group and Artemisinin ＋ Aβ 1-42 group. The proliferation of cells was detected by cell proliferation assay. The expression of ROS in cells was assessed by immunofluorescence. Lactate dehydrogenase cytotoxicity assay was used to test cell damage. The protein expression of Nrf2 and HO-1 was analyzed by Western blotting. Results Compared with the control group,Artemisinin attenuated damage and the inhibitory effect on the proliferation activity induced by Aβ 1-42 in SH-SY5Y cells. In addition,Artemisinin inhibited ROS induced by Aβ 1-42 and upregulated the protein expression of Nrf2 and HO-1 in SH-SY5Y cells. Conclusion Artemisinin can improve the cytotoxic effect of Aβ 1-42 -induced oxidative stress on SH-SY5Y cells through the Nrf2/HO-1 pathway.