通络驻景丸对糖尿病大鼠视网膜的保护作用研究

摘要

目的 探讨通络驻景丸对糖尿病大鼠视网膜的保护作用及其作用机制.方法 以腹腔注射链脲佐菌素(STZ)建立糖尿病动物模型,建模成功动物随机分为模型对照组(DM组)、通络驻景丸组(TLZJ组),各20只,另选择大鼠20只为空白对照组(NC组). NC组、DM组给予蒸馏水灌胃,TLZJ组给予通络驻景丸水煎剂灌胃,于6周和12周时,应用免疫组织化学染色法和实时聚合酶链反应Real-time PCR检测各组大鼠视网膜中Nrf2、HO-1、VEGF蛋白及mRNA的表达量.结果 各组Nrf2、HO-1、VEGF蛋白及mRNA的表达具有一致性.6周和12周时,DM组Nrf2、HO-1、VEGF 的表达量较NC 组增加 (P=0.000,P＜0.05);TLZJ 组Nrf2、HO-1的表达量较DM组增加,VEGF的表达量降低 (P=0.000,P＜0.05);12周与6周比较,DM组Nrf2、VEGF的表达量较6周增加,HO-1 表达量降低 (P=0.000,P＜0.05);TLZJ 组Nrf2、HO-1的表达量较6周增加,VEGF表达量降低(P=0.000,P＜0.05).结论 通络驻景丸可有效减轻DM大鼠视网膜组织氧化应激损伤、抑制视网膜细胞增殖,可能与Nrf2/ARE通路的激活以及Nrf2、HO-1、VEGF蛋白表达有关.%OBJECTIVE To investigate the protective effects of Tongluo Zhujing pill on retina of rats with diabetes mellitus and its underlying mechanism. METHODS The diabetic model was established by intraperitoneal injection of streptozotocin (STZ). The model rats were randomly divided into model control group (DM group) and Tongluo Zhujing group (TLZJ group) with 20 rats in each group. Another 20 rats were assigned into normal control (NC) group. Rats in NC group and DM group were given distilled water by gavage, animals in TLZJ group were given Tongluo Zhujing decoction intragastrically. Six weeks and 12 weeks afterwards, immunohisto-chemical method and real-time quan-titative PCR were used respectively to detect the relative expression levels of Nrf2, HO-1 and VEGF in retinas of the rats. RESULTS The expressions of Nrf2, HO-1 and VEGF in different group were in consistency. Six weeks and twelve weeks after intervention , the expressions of each factor in DM group were higher than those in the NC group.The Nrf2 and HO-1 in TLZJ group were higher than those in the DM group,but the VEGF was lower than its counterparts (P＜0.05).After 12 weeks,the expressions of VEGF and Nrf2 in DM group were more than those indexes detected 6 weeks after treatment,but the HO-1 was lower; the Nrf2 and HO-1 in TLZJ group were higher than counter-parts at the prior time point, and the VEGF was lower (all P＜0.05).CONCLUSIONS Tongluo Zhujing pill effectively relieved oxidative stress injury and inhibited retinal proliferation in retina of DM rats, which might be related to the activation of Nrf2/ARE pathway and the expression of Nrf2, HO-1 and VEGF.