Nrf2-ARE信号通路参与姜黄素对Aβ诱导细胞氧化损伤和凋亡的抑制作用研究

发布时间：2018-10-30 08:42

【摘要】：本文研究了Nrf2-ARE通路在姜黄素介导的抑制β-淀粉样蛋白(Aβ)诱导SH-SY5Y细胞氧化损伤及细胞凋亡过程中的作用。在没有/含有姜黄素预先保护情况下,10μM Aβ培养细胞24 h,观察细胞形态的变化,测定细胞存活率、细胞乳酸脱氢酶(LDH)释放水平,评价细胞培养液中H2O2及胞内活性氧水平,SDS-PAGE酶联免疫法测定Nrf2、HO-1蛋白表达水平。结果表明,与对照组相比,Aβ损伤组细胞突起变少、变短,胞体变圆,细胞存活能力降低、释放LDH的水平明显增加、氧化应激水平明显上升。与Aβ损伤组相比,姜黄素保护组细胞胞体突起较多、较长,细胞存活能力明显升高、释放LDH的水平明显降低、氧化应激水平也明显降低。姜黄素增强了Nrf2的表达,降低了Aβ诱导的Nrf2 Ser-40磷酸化及HO-1的相对表达水平。以上结果提示,姜黄素能够削弱Aβ诱导的氧化损伤和细胞凋亡作用,这可能与姜黄素对Nrf2-ARE通路的活性调节相关。
[Abstract]:The role of Nrf2-ARE pathway in curcumin mediated inhibition of oxidative damage and apoptosis of SH-SY5Y cells induced by 尾 -amyloid protein (A 尾) was studied. In the absence of / containing curcumin, the cells were cultured at 10 渭 Ma 尾 for 24 h. The cell morphology was observed, the cell survival rate, the level of lactate dehydrogenase (LDH) release, and the levels of H2O2 and reactive oxygen species (Ros) in the cell culture medium were evaluated. SDS-PAGE enzyme linked immunosorbent assay (SDS-PAGE) was used to detect the expression of Nrf2,HO-1 protein. The results showed that compared with the control group, the cells of A 尾 injured group had fewer processes, shorter cell bodies, lower cell viability, higher levels of LDH release, and higher levels of oxidative stress. Compared with A 尾 injury group, curcumin protected cells had more and longer somatic processes, higher cell viability, lower level of LDH release and lower oxidative stress. Curcumin enhanced the expression of Nrf2 and decreased the A 尾 -induced Nrf2 Ser-40 phosphorylation and the relative expression of HO-1. These results suggest that curcumin can attenuate the oxidative damage and apoptosis induced by A 尾, which may be related to the regulation of curcumin on the activity of Nrf2-ARE pathway.
【作者单位】：北京联合大学生物活性物质与功能食品北京市重点实验室;北京联合大学应用文理学院;
【基金】：国家自然科学基金资助项目(31471587) 北京市属高等学校高层次人才引进与培养计划项目(CIT&TCD201504034) 北京联合大学“启明星”大学生科技创新项目(201511417015)
【分类号】：R749.16;TS201.4

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