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姜黄素抑制小胶质细胞NADPH氧化酶保护多巴胺能细胞的机制研究 被引量:1

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摘要 目的探讨小胶质细胞在多巴胺能细胞损伤中的作用,以及姜黄素通过抑制小胶质细胞反应保护多巴胺能细胞的机制。方法选用大鼠嗜铬细胞瘤株PC12细胞,用鱼藤酮诱导其损伤建立帕金森病细胞模型;用姜黄素预处理4h的BV-2细胞再经鱼藤酮处理4h后的细胞上清液作为条件培养液(microglia conditioned medium with curcumin,MCMC),处理PC12细胞。应用四甲基偶氮唑盐法(MTT法)检测细胞活力;DCFH-DA染色检测BV-2细胞内活性氧类物质(ROS)的水平;Western blotting法检测NADPH氧化酶P47-phox亚基在BV-2细胞膜上的表达。结果与对照组相比,经姜黄素预处理的BV-2细胞ROS水平降低(P<0.01);受MCMC处理的PC12细胞活力增加(P<0.01)。姜黄素预处理使结合到BV-2细胞膜的NADPH氧化酶P47-phox亚基明显降低(P<0.05)。结论鱼藤酮通过激活小胶质细胞内NADPH氧化酶产生ROS,损伤多巴胺能细胞。姜黄素能够抑制小胶质细胞内NADPH氧化酶的激活,减少ROS的产生,进而保护多巴胺能细胞。
作者 崔群力
出处 《中国实用神经疾病杂志》 2015年第11期37-39,共3页 Chinese Journal of Practical Nervous Diseases
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