Objective: To observe the effects of Shenshuai II Recipe (SSR) on the fibrosis of remnant nephridial tissue and expressions of Ang II and nNOS in the chronic renal failure (CRF) rats induced by 5/6 ablation/infarction (A/I), and to preliminarily investigate its mechanism of action.
Methods: Fifty-seven SD male rats were used to prepare the CRF rat model by means of 5/6 A/I. After modeling, they were randomly divided into the model group, the SSR group (2 mL SSR condensed decoction given by gastrogavage), and the Western medicine group (treated by 2 mL suspension of losartan potassium and fosinopril sodium given by gastrogavage), 15 rats in each group. Another 15 rats were recruited as the normal control group. Equal volume of pure water was given to rats in the normal control group and the model group. Relevant treatment was given to rats in each group once daily, for 60 successive days. The serum creatinine (SCr), blood urea nitrogen (BUN), and creatinine clearance rate (CCr) were detected. The expressions of angiotensin II (Ang II) and nervous system type nitric oxide synthase (nNOS) in the remnant renal cortex and the medulla were detected by Western blot. The pathomorphology of the nephridial tissue was observed.
Results: Compared with the normal control group, the levels of SCr and BUN increased (P<0.01) and the level of CCr decreased (P<0.01) in the model group, indicating a successful modeling. Compared with the same group before treatment, the levels of SCr and BUN decreased and the level of CCr increased in the SSR group and the Western medicine group (all P<0.01). Compared with the model group after treatment, the levels of SCr and BUN decreased, and the expression of Ang II in the medulla decreased in the SSR group and the Western medicine group (P<0.01, P<0.05). The levels of CCr and protein expressions of nNOS in the renal cortex and the medulla obviously increased in the SSR group and the Western medicine group (P<0.01, P<0.05). The pathology of the nephridial tissue showed that the pathological changes in the SSR group were obviously ameliorated, better than those of the model group.
Conclusions: SSR could improve the renal function and relieve the renal interstitial fibrosis in the rats induced by 5/6 A/I. Its mechanism of action was possibly correlated with regulating the renal imbalanced Ang II and nNOS signal transduction pathway.
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