溺毒清合剂对慢性肾衰竭大鼠纤维化指标的影响

Influence of Niduqing on fibrosis index of chronic renal failure rats

目的:探讨溺毒清合剂延缓慢性肾衰的作用机理。方法:采用5/6肾切除造模方法复制大鼠慢性肾功能衰竭模型,实验分为假手术组、模型组、溺毒清低剂量组(简称溺低组)、溺毒清高剂量组(简称溺高组)、厄贝沙坦对照组(简称厄贝组)。对各组进行干预治疗,然后观察其肾功能变化。并对肾组织经行IV胶原、FN(纤维连接蛋白)、TGF-β(转化生长因子-β)等免疫组化检测,最后行肾组织病理检查。结果:溺毒清合剂可显著改善CRF大鼠肾功能,改善肾功能方面与厄贝沙坦相当。免疫组化显示溺毒清高剂量组比模型组IV胶原、FN、TGF-β表达减少。结论:溺毒清合剂可显著改善CRF大鼠的肾功能,通过降解Ⅳ型胶原等细胞外基质而抑制5/6肾切除大鼠残肾组织肾小球硬化,从而延缓慢性肾衰进展,与厄贝沙坦有相近的肾脏保护作用。

Objective：To explore the mechanism of the therapeutic effect of Niduqing on experimental chronic renal failure （CRF）. Methods：Fifty male SD rats were made into CRF model by 5/6 nephrectomy and were randomly sorted into following groups ： model group, Niduqing low and high dose groups, Erbesartan group and sham - operation group. By the end of the second month, the rats were killed. The change of renal function was observed and IV collagen, FN and TGF - 13 in nephridial tissue were detected by SABC, then the pathologic changes in renal tissue were observed by light microscopy. Results ： Niduqing can improve the renal function of CRF fats as Erbesartan does. IV collagen, FN and TGF - β expressions decreased in Niduqing high dose group. Conclusion ： Niduqing can significantly improve the renal function of CRF fats and inhibit glomerulosclerosis in CRF fats by degrading extracellular matrix （ECM）, thus delaying the progress of CRF, which has similar renal protection as Erbesartan.