盐酸吡格列酮对糖尿病大鼠肾组织TOLL 受体4 / MAPKs 信号通路的影响

目的:探讨吡格列酮对糖尿病肾病大鼠肾组织中TOLL 受体4/ MAPKs 信号通路的影响。方法:将雄性SD 随机分为对照组(n =8)和试验组(n =32)。试验组SD 鼠造模成功后随机分为3 组进行干预,应用Western blot 检测对照组和干预组大鼠肾组织中丝裂原活化蛋白激酶ERK1/2 及p38MAPK 磷酸化水平。结果:与对照组比较,各组大鼠肾组织中TOLL 受体4 表达增强,其中ERK1/2 与JNK 磷酸化水平明显升高(P<0郾05),但p38MAPK 水平变化不明显(P>0郾05);与模型组比较,吡咯列酮干预组大鼠肾组织中ERK1/2 与p38MAPK 磷酸化水平降低(P<0郾05)。结论:吡格列酮通过TOLL 受体4/ MAPKs/ERK1/2 与TOLL 受体4/ MAPKs/ JNK 信号通路来完成,延缓糖尿病肾病的发生与发展。

Role of TOLL-like receptor 4 / MAPKs pathway of renal tissue in diabetic rats by pioglitazone

Objective:To study the role of TOLL-like receptor4/ MAPKs pathway of renal tissue in the diabetic rats treated with Piogitazone.Methods:The male Sprague Dawlry rats were randomly selected as the control group (n =8) and experimental group(n =32).The experimental rats were randomly divided into three groups.The expression of ERK1/2,JNK and p38MAPK,and levels of their phosphorylation in kidney were measured by Western blot in control group and experimental group.Results:The expression of TOLL- like receptor 4 in all renal tissue in the diabetic rats were significantlyincreased than those in control group (P<0.01).Compared with the control group.The activity of p-ERK1/2 and p38MAPK significantly increased in each experimental group (P <0.05),but the expression level of p-JNK was no statistical significance.TOLL-like receptor 4 could regulatory effect on the phorylation of ERK1/2 and p38MAPK. Compared with the model group,the expression of p-ERK1/2 and p38MAPK significantly decreased(P<0.05),moreover, these changes were more significant in high-dose treated group (P<0.05).Conclusion:Pioglitazone inhibits the expression of TOLL-like receptor 4 of renal tissue in the diabetic rats,and these effects may be related to TOLL-like receptor 4/ ERK1/2 and TOLL-like receptor 4/ p38MAPK pathways.