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目的:进一步探讨糖肾颗粒对2型糖尿病大鼠肾脏的保护作用及从炎症角度探讨其机制。方法:SD大鼠随机分为正常对照组、糖尿病模型组和糖肾颗粒治疗组(含生药21g/kg)。以高脂高糖饮食加低剂量注射链脲佐菌素(STZ,30 mg/kg)复制2型糖尿病大鼠模型。观察各组生化指标,光镜(HE和PAS染色)观察肾脏病理,免疫组化技术检测转化生长因子β1(TGFβ1)蛋白表达,荧光定量PCR技术检测肾脏组织中TGFβ1 mRNA表达,ELISA技术检测血清巨噬细胞趋化因子1(MCP-1)、细胞间黏附分子1(ICAM-1)和肿瘤坏死因子α(TNFα)的浓度。结果:实验8周末,模型组血糖、胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL)、24h尿微量蛋白(Ualb)均升高,肾脏TGFβ1蛋白和mRNA表达增加,血液中MCP-1、ICAM-1和TNFα水平均增高,与正常对照组比较,均P<0.01;肾间质炎症细胞浸润。与模型组比较,糖肾颗粒治疗可改善生化指标P<0.05;减轻肾脏病变及炎症细胞浸润;抑制TGFβ1基因和蛋白的表达,P<0.05;降低血液中炎症因子的含量,ICAM-1和TNFα,P<0.05。结论:糖肾颗粒对糖尿病肾脏具有保护作用,其部分机制可能通过抑制炎症因子的释放,减少炎症细胞浸润实现的。
Objective: To further explore the protective effects of Tangshen Granule on the kidney of type 2 diabetic rats and to explore its mechanism from the perspective of inflammation. Methods: SD rats were randomly divided into normal control group, diabetic model group and Tangshen Granule group (containing crude drug 21g / kg). Type 2 diabetic rat models were reproduced with high-fat and high-sugar diet plus low-dose streptozotocin (STZ, 30 mg / kg). The pathological changes of kidney were observed by light microscopy (HE and PAS staining), the expression of transforming growth factor β1 (TGFβ1) was detected by immunohistochemistry, the expression of TGFβ1 mRNA was detected by fluorescence quantitative PCR, The concentrations of MCP-1, ICAM-1 and TNFα were measured. Results: At the end of the experiment, blood glucose, cholesterol (TC), triglyceride (TG), low density lipoprotein (LDL) and urinary microalbuminuria (Ualb) increased and the expression of TGFβ1 protein and mRNA increased in the model group MCP-1, ICAM-1 and TNFα levels were increased, compared with the normal control group, P <0.01; interstitial inflammatory cell infiltration. Compared with the model group, Tangshen Granule could improve the biochemical indexes (P <0.05), reduce the renal lesions and inflammatory cell infiltration, inhibit the expression of TGFβ1 gene and protein, P <0.05, reduce the levels of inflammatory cytokines, ICAM-1 and TNFα , P <0.05. Conclusion: Tangshen Granule has a protective effect on diabetic nephropathy, and some of its mechanisms may be through inhibiting the release of inflammatory factors and reducing inflammatory cell infiltration.