固冲汤对IgA肾病模型大鼠肾组织TGF-β1含量及病理形态的影响

Effect of Guchong Decoction on TGF-β1 content and pathological morphology in renal tissue of IgA nephropathy model rats

目的观察固冲汤对IgA肾病模型大鼠肾组织病理变化的影响,探讨可能的作用机制。方法将SD大鼠采用随机数字表法分为正常组、模型组、福辛普利组、固冲汤组,每组10只。采用BSA+葡萄球菌肠毒素B(SEB)法构建IgA肾病大鼠模型。固冲汤组灌服固冲汤水煎浓缩液,福辛普利组灌服福辛普利水溶液,正常组及模型组予等量的生理盐水灌胃。干预后12周处死。HE染色法、Masson染色法、PAS染色法观察肾脏组织病理改变和IgA的沉积情况,免疫荧光法检测肾组织,ELISA法检测肾脏组织TGF-β1表达。结果与正常组比较,福辛普利组、固冲汤组大鼠肾组织TGF-β1表达明显增强(P<0.05);与模型组比较,正常组TGF-β1表达较弱(P<0.05);与模型组比较,固冲汤组大鼠肾组织TGF-β1表达明显减弱(P<0.05)。福辛普利组及固冲汤组与模型组相比,肾脏病变较轻。结论固冲汤对肾脏的保护机制可能与抑制TGF-β1的表达、减少细胞外基质生成有关。

Objective To explore the effect of Guchong Decoction on the pathological changes in renal tissue of IgA nephropathy model rats,and explore the possible mechanism.Methods Forty female SD mice were randomly divided into 4 groups:normal group,model group,Guchong Decoction group(GD group)and fosinopril tablets group(FT group),10 rats in each group.The model of IgA nephropathy was established by oral BSA+intravenous injection of SEB.GD group was given concentrated solution of Guchong Decoction,FT group was given fosinopril solution,and the normal group and model group were given the same volume of normal saline by gavage.Mice were sacrificed after 12 weeks of treatment.The pathological changes in renal tissue and the deposition of IgA were observed by HE staining,Masson stainning and PAS staining.Immunofluorescence was used to detect renal tissues.ELISA was used to detect the expression of TGF-β1 in the kidney.Results Compared with normal group,the expression of TGF-β1 in renal tissue of FT group and GD group was significantly increased(P<0.05);compared with model group,the expression of TGF-β1 in control group was weaker(P<0.05);Compared with model group,the expression of TGF-β1 in the renal tissue of GD group was significantly reduced(P<0.05).Compared with model group,the damage in kidney in FT group and GD group was milder.Conclusion The protective mechanism of Guchong Decoction on kidney may be related to the inhibition of TGF-β1 expression and the reduction of extracellular matrix production.