论文部分内容阅读
目的:观察尿毒康对慢性肾衰阳虚型模型大鼠肾纤维化的影响。方法:40只SD雄性大白鼠随机抽取10只作为正常对照组,其余30只采用5/6肾切除改良法配合丙基硫氧嘧啶灌胃制成慢性肾衰阳虚模型。造模成功后,再随机分为慢性肾衰阳虚组以及尿毒康组各15只。8周后处死大鼠取肾脏进行免疫组织化学染色,检测Ⅳ型胶原、纤维连接蛋白(FN)、转化生长因子β_1(TGFβ_1)、基质金属蛋白酶-2(MMP_2)在肾组织中的表达。结果:与正常对照组比较,慢性肾衰阳虚组Ⅳ型胶原、FN、TGFβ_1均表达较强(P<0.01),而MMP_2表达较弱(P<0.01);与慢性肾衰阳虚模型组比较,尿毒康组Ⅳ胶原、FN、TGFβ_1的表达均明显较弱(P<0.05,P<0.01),MMP_2表达较强(P<0.05)。结论:尿毒康能减轻慢性肾衰阳虚型大鼠肾纤维化,作用机制可能与上调MMP2的表达及降低TGFβ_1表达有关。
Objective: To observe the effect of Ureukang on renal fibrosis in chronic kidney failure model rats with yang deficiency. METHODS: Forty male SD rats were randomly selected as normal control group and the remaining 30 rats were treated with 5/6 nephrectomy and propylthiouracil to establish a chronic kidney failure yang deficiency model. After the model was successfully established, they were randomly divided into chronic kidney failure Yang deficiency group and uremic XK group. After 8 weeks, the rats were sacrificed and the kidneys were taken for immunohistochemical staining. The expression of type IV collagen, fibronectin (FN), transforming growth factor β 1 (TGFβ 1), and matrix metalloproteinase-2 (MMP 2) was detected in kidney tissue. Results:Compared with the normal control group, the expression of type IV collagen, FN, TGFβ_1 in chronic kidney failure yang deficiency group was stronger (P<0.01), while the expression of MMP_2 was weaker (P<0.01); it was associated with chronic kidney failure Yang deficiency model group In comparison, the expression of collagen IV, FN and TGFβ_1 in Uyukemia group was significantly weaker (P<0.05, P<0.01), and the expression of MMP_2 was stronger (P<0.05). Conclusion: Ureukang can reduce renal fibrosis in rats with chronic kidney failure. The mechanism may be related to the up-regulation of MMP2 expression and the decrease of TGFβ_1 expression.