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目的探讨熊果酸预处理对视网膜缺血-再灌注损伤的保护作用及作用机制。方法随机选取60只大鼠,随机均分为假手术组,视网膜缺血-再灌注损伤组,熊果酸(10、20、40mg·kg~(-1))3个剂量组和α硫辛酸阳性对照组。采用前房灌注法建立大鼠视网膜缺血-再灌注损伤模型。电生理检测仪检测视网膜电图b波振幅,HE染色观察视网膜厚度,流式细胞仪检测视网膜细胞凋亡率,罗丹明染色检测线粒体膜电位,Western blotting检测p53,Bcl-2和Bax蛋白。结果熊果酸预处理可明显增加视网膜电图b波振幅、视网膜厚度以及线粒体膜电位和Bcl-2表达,明显减少视网膜细胞凋亡以及下调Bax和p53表达。结论熊果酸预处理可通过抑制线粒体凋亡通路而减轻视网膜缺血再灌注损伤,其作用机制与下调p53的表达相关。
Objective To investigate the protective effect and mechanism of ursolic acid preconditioning on retinal ischemia-reperfusion injury. Methods Sixty randomly selected rats were randomly divided into three groups: sham operation group, retinal ischemia - reperfusion injury group, ursolic acid (10, 20 and 40 mg · kg -1) Positive control group. Rat models of retinal ischemia-reperfusion injury were established by anterior chamber perfusion. The electrophysiological detector was used to detect the b wave amplitude. The thickness of retina was observed by HE staining. The apoptosis rate of retinal cells was detected by flow cytometry. The mitochondrial membrane potential was detected by rhodamine staining. The protein expressions of p53, Bcl-2 and Bax were detected by Western blotting. Results UA could significantly increase the b-wave amplitude, retinal thickness, mitochondrial membrane potential and Bcl-2 expression, significantly reduce retinal cell apoptosis and down-regulate the expression of Bax and p53. Conclusion UA can reduce retinal ischemia-reperfusion injury by inhibiting the mitochondrial apoptosis pathway, and its mechanism may be related to the down-regulation of p53 expression.