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目的:通过动物实验,基于免疫炎性反应因子MCP-1、TGF-β,探索益气活血散结法改善肾小球硬化的分子机制。方法:24只GK大鼠,随机分为模型组、假手术组、益气活血散结组。通过高脂高能量喂养加单肾切除术复制糖尿病肾病模型。检测各组大鼠的24 h尿蛋白,观察大鼠在干预后肾脏组织的病理改变,同时采用Western blotting以及免疫组化法检测肾脏组织的MCP-1和TGF-β的表达情况,采用RT-PCR法检测MCP-1mRNA以及TGF-βmRNA的表达水平。结果:PASM染色和Masson染色显示:益气活血散结组阳性率明显低于模型组(P<0.01)。益气活血散结组中24 h尿蛋白在药物干预后明显减少(P<0.01)。Western blotting、免疫组化结果均显示:益气活血散结组MCP-1(P<0.05)、TGF-β(P<0.01)的表达程度明显低于模型组。同样,RT-PCR结果也显示:MCP-1mRNA(P<0.01)、TGF-βmRNA(P<0.05)水平在益气活血散结组明显低于模型组。结论:益气活血散结法可以有效地减少24 h尿蛋白定量、延缓肾小球纤维化,其机制可能与抑制肾脏组织中MCP-1和TGF-β的表达有关。
OBJECTIVE: To explore the molecular mechanism of Yiqi Huoxue Sanjie to improve glomerulosclerosis through animal experiments based on immune-inflammatory response factors MCP-1 and TGF-β. Methods: Twenty-four GK rats were randomly divided into model group, sham operation group and Yiqi Huoxue Sanjie group. Diabetic nephropathy model was reproduced by high fat and high energy feeding plus nephrectomy. The 24 h urinary protein was detected in each group, and the pathological changes of kidney in rats were observed. The expressions of MCP-1 and TGF-β in kidney were detected by Western blotting and immunohistochemistry. PCR method was used to detect the expression of MCP-1mRNA and TGF-βmRNA. Results: PASM staining and Masson staining showed that the positive rate of Yiqi Huoxue Sanjie group was significantly lower than that of model group (P <0.01). The 24 h urine protein in Yiqi Huoxue Sanjie group was significantly decreased after drug intervention (P <0.01). Western blotting and immunohistochemistry showed that the expression of MCP-1 (P <0.05) and TGF-β (P <0.01) in Yiqi Huoxue Sanjie group were significantly lower than those in model group. Similarly, the results of RT-PCR also showed that the levels of MCP-1 mRNA (P <0.01) and TGF-βmRNA (P <0.05) were significantly lower in Yiqi Huoxue Sanjie group than in model group. Conclusion: Yiqi Huoxue Sanjie Decoction can effectively reduce 24 h urinary protein and delay glomerular fibrosis, the mechanism may be related to the inhibition of the expression of MCP-1 and TGF-β in kidney tissue.