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

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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(P0.05);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<0.05)。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。“,”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.
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