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目的:研究柯里拉京对活性氧诱导小鼠小胶质细胞N9氧化损伤的保护作用。方法:以叔丁基过氧化氢(tert-butyl hydroperoxide,t-BHP,0.6 mM)孵育24 h损伤N9细胞建立活性氧氧化应激模型;以柯里拉京(0.5~4μM)预孵育24 h进行干预,通过光镜观察细胞形态差异,MTT法检测细胞活力,罗丹明123染色法检测细胞线粒体膜电位(mitochondrial membrane potentials,MMP),硫代巴比妥酸法测定丙二醛(malondialdehyde,MDA)含量等观察柯里拉京预处理的保护作用。结果:与氧化损伤模型组比较,柯里拉京预处理能明显提高t-BHP诱导损伤的N9细胞活力,改善损伤的N9细胞形态,显著抑制t-BHP引起的MMP降低和MDA升高。结论:柯里拉京能够抑制活性氧对N9细胞的氧化损伤,其保护作用可能与其抑制氧化应激引起线粒体功能损伤有关。
AIM: To investigate the protective effect of flocculant on oxidative damage induced by reactive oxygen species (NOS) in mouse microglial cells. Methods: Oxidative stress model was established by incubating N9 cells with tert-butyl hydroperoxide (t-BHP, 0.6 mM) for 24 h. Preincubation with Corilagin (0.5 ~ 4 μM) The morphological changes of cells were observed by light microscope. Cell viability was measured by MTT assay. Mitochondrial membrane potentials (MMPs) were detected by rhodamine 123 staining. Malondialdehyde (MDA) Content observed corilagin preconditioning protective effect. RESULTS: Corilagin preconditioning significantly increased the viability of N9 cells induced by t-BHP, and improved the morphology of injured N9 cells. The pretreatment with corilagin significantly inhibited the decrease of MMPs and the increase of MDA induced by t-BHP. CONCLUSION: Corilagin can inhibit the oxidative damage of N9 cells by reactive oxygen species, and its protective effect may be related to the inhibition of mitochondrial function damage induced by oxidative stress.