补肾活血方对肾小球硬化大鼠细胞外基质状态的影响

目的 探讨补肾活血方对肾小球硬化大鼠细胞外基质状态的影响及作用机制。 方法 采用单侧肾切除加注射阿霉素造模法，将实验动物随机分为正常组、模型组、中药补肾活血方组（中药组）、西药福辛普利钠对照组（西药组），每组11只。分别灌胃给药及生理盐水8周后，观察大鼠24 h尿蛋白及肾功能，采用免疫组化法检测肾组织中基质金属蛋白酶-1（MMP-1）、组织蛋白酶抑制剂-1（TIMP-1）的表达，ELISA检测血浆和肾组织中转化生长因子-β1（TGF-β1）的含量。 结果 与正常组比较，模型组大鼠24 h尿蛋白明显增多，肾功能下降；肾组织中TIMP-1表达增加，MMP-1表达下降，半定量结果显示模型组与正常组比较差异有统计学意义（P <0.05）；中药组和西药组均能降低肾组织TIMP-1含量，提高MMP-1含量，与模型组比较，差异有统计学意义（P <0.05）。与正常组比较，模型组大鼠血和肾组织的TGF-β1含量明显升高（P <0.01），中药组血和肾组织的TGF-β1含量较模型组低，但差异无统计学意义

Effect of Bushen Huoxue Recipe on the State of Extracellular Matrix in Glomerulosclerosis Rats Model

Objective To investigate the effect and acting mechanism of Bushen Huoxue Recipe（BHR） on the state of extracellular matrix in glomerulosclerosis（GS） rats model.Methods GS rat model was established by unilateral nephrectomy and adriamycin injection.Model rats were randomly divided into 4 groups： the normal control group,the model group,the test group treated by BHR,and the positive control group treated with fosinopril sodium,with 11 rats in each group.The 24 h urinary protein and renal function of rats were observed,the contents of matrix metalloproteinase 1（MMP-1）,tissue inhibitor of metalloproteinase 1（TIMP-1） in renal tissue and transforming growth factor-β1（TGF-β1） in blood plasma,and renal tissue were detected.Results Compared with those in the normal control group,24 h urinary protein was increased and renal function was deprived in the model group;TIMP-1 expression increased,MMP1 expression decreased in renal tissue of rats in the model group,showing statistical difference between groups（P0.05）.As compared with the model group,the abnormal changes of TIMP-1 and MMP1 expressions were ameliorated in the two groups treated either by BHR or fosinopril（P0.05）.The content of TGF-β1 in the model group,either in blood or in renal tissue,was significantly higher than those in the normal control group respectively（P0.01）,showing no significant change after BHR treatment.Conclusion The protective effect of BHR on renal function in rats with GS is possibly by way of influencing expressions of TGF-β1,TIMP-1 and MMP1 to regulate the state of extracellular matrix and lessen the matrix aggregation.