中文摘要：

目的：通过观察肾衰饮对慢性肾功能衰竭大鼠肾脏TNF-α的表达及MAPK通路相关蛋白的检测,探讨肾衰饮抗肾纤维化的调控机制。方法：采用腺嘌呤肾病模型,以尿毒清组作为对照,观察肾衰饮对CRF大鼠TNF-α的影响。通过ELISA法检测TNF-α的表达,Western Blot（WB）法检测p-p38、p-JNK、p-ERK的蛋白表达。结果：与正常组比较,模型组SCr、BUN水平显著升高（P〈0.01）;与模型组比较,肾衰饮组和尿毒清组大鼠SCr、BUN水平均显著降低（P〈0.01）。HE染色提示：肾衰饮及尿毒清能够改善模型组大鼠肾脏病理学改变。ELISA结果提示：模型组与正常组比较TNF-α表达明显增强,TNF-α升高（P〈0.01）,治疗后肾衰饮组TNF-α表达明显减少（P〈0.01）。WB结果显示,肾衰饮可下调p-p38、p-JNK、p-ERK的蛋白表达（P〈0.01）。结论：肾衰饮可能分别通过调控p38、JNK、ERK通路,抑制TNF-α的表达,以抑制肾纤维化的发生、发展。

英文摘要：

Objective：By observing the effect of Shenshuaiyin on chronic renal failure rats renal expression of TNF - α and MAPK pathways related protein to explore the regulatory mechanism of Shenshuaiyin in anti - renal fibrosis. Methods ： Adenine ne- phropathy model was set up and poisonous clear urine was as a control group. Observe Shenshuaiyin influence of TNF - α on CRF rats. Use the ELISA method to detect the expression of TNF-α and Western Blot （WB） method to detect the p -p38, p -JNK and p - ERK protein expressions. Results ： Comparing with the control group, the levels of serum creatinine and urea nitrogen in- creased significantly （ P 〈 0. 01 ） in model group. Comparing with the model group, the levels of serum creatinine and urea nitro- gen decreased significantly （P 〈0. 01 ）in Shenshuaiyin group and Niaoduqiug group. HE dyeing showed that there has obvious pathological changes in the kidney tissue in model group. ELISAresults showed that the model group significantly enhanced TNF -α expression compared with the normal group （P 〈 0. 01 ）. After the treatment of Shenshuaiyin, TNF-α expression decreased significantly（ P 〈 0. 01 ）. WB results showed that Shenshuaiyin can decrease the protein expressions of p- p38 ,p -JNK and p - ERK （P 〈 0. 01 ）. Conclusion：Shenshuaiyin may suppress the occurrence and development of renal fibrosis respectively through regulating p38, JNK and ERK pathway,inhibiting the expression of TNF- α.