丹参预处理对大鼠视网膜缺血再灌注损伤的作用及对Bcl-2表达的影响

Protective effect and Bcl-2 expression of salvia miltiorrhiza pretreatment on retinal ischemia-reperfusion injury

目的探讨大鼠视网膜缺血再灌注损伤(RIRI)过程中,丹参对视网膜缺血再灌注损伤的保护作用以及对Bcl-2蛋白表达的影响。方法随机选取132只Wistar大鼠,分为正常对照组、缺血再灌注组、丹参预处理组,通过对前房加压制作视网膜缺血再灌注损伤模型,后2组再各根据不同的缺血再灌注时间(6 h、12 h、24 h、48 h、72 h)分为5个亚组。HE染色观察其视网膜组织学变化,SABC法和Western-blot法检测Bcl-2蛋白表达的变化。结果 Bcl-2蛋白在正常组表达较弱,在缺血再灌注组和丹参预处理组缺血再灌注6 h后开始表达,24 h后显著增强,48 h后下降,72 h后表达减弱,变化趋势基本一致。但是2组比较,丹参预处理组在不同时间点Bcl-2蛋白的表达均明显强于缺血再灌注组,差异具有统计学意义(P<0.01)。结论丹参预处理对视网膜缺血再灌注损伤可以通过减少神经节细胞的凋亡起到保护作用,其作用机制可能是通过调节Bcl-2蛋白的表达来实现。

Objective To study the protective effect and Bcl-2 expression of salvia miltiorrhiza pretreatment on retinal ischemia-reperfusion injury（ RIRI）. Methods One hundred and thirty two Wistar rats were randomly divided into the normal control group,the ischemiareperfusion group and the salvia miltiorrhiza pretreatment group. The model of retinal ischemia-reperfusion injury was constructed by increasing the intraocular pressure. The ischemia-reperfusion and salvia miltiorrhiza pretreatment group were divided into five subgroups according to the different reperfusion time（ 6 h,12 h,24 h,48 h and 72 h）. Observe the histological changes in retina by HE staining. The SABC（ strept avidin-biotin complex） and Western-blot were used to measure changes of Bcl-2 protein levels in retinal. Results The positive expression of Bcl-2 protein was weak in normal group. In the ischemia-reperfusion group and salvia miltiorrhiza pretreatment group,the expression of Bcl-2 protein began to increase at 6 hours after reperfusion,reached the peak at 24 hours after reperfusion,began to decrease at 48 hours after reperfusion,and started to weaken at 72 hours after reperfusion. The variation tendency of the two groups were the same,however,the expression of Bcl-2 was significantly stronger in the salvia miltiorrhiza pretreatment group compared with ischemia-reperfusion group,and there was significant difference between the two groups（ P〈0. 01）. Conclusion Salvia miltiorrhiza pretreatment can protect the retina by reducing retinal ganglion cells apoptosis in retinal ischemia-reperfusion injury. The mechanism may be achieved by regulating the expression of Bcl-2 protein.