The Theoretical And Experimental Study On The Therapy Of The Mediating Jue-yin Improving Chronic Renal Failure Rat

Objective:To discusse the correlation of pathogenesis of chronic renal failure (CRF) with Jueyin disease, the thinging of treating chronic renal failure by mediating-Jueyin, and study the mechanism of the method of mediating-Jueyin interfering in renal fibrosis.Methods:Put fotward the hypothesis that CRF are resulted from Jueyin helm malfunction. Take mediating-Jueyin as treatment method, composing the formula rationally, choosing the medicine carefully, to make the Reconciliating Collaterals and Dispersing Turbid Granula(RDG). Using 5/6 nephrectomy rats divided into 6 groups, which are normal group, model group, treated by Fuxinpuli group, treated by RDG Low-dose group(group I),RDG middle-dose group(group II) and RDG High-dose group(group III). Observing the weight change of the rat and their biochemical results:blood urea nitrogen(BUN), serum creatinine(Scr). Take the renal tissue from the operative side. HE staining and immunohistochemical methods were used to detect the changes of Fibronectin (FN). immunohistochemical and RT-PCR methods were used to detect the changes of the gene and protein expression of transforming growth factor-β1/Smad singaling Pathway (TGF-β1/Smads).Result:Compared with the untreated 5/6 nephrectomized group, BUN,Scr of RDG groups and Fuxinpuli group were substantially decreased (P< 0.05). The expression of TGF-β1,p-Smad2/3,FN in 5/6 nephrectomy rats is higher than in normal group. It was less in RDG groups and Fuxipuli group (P< 0.05).The expression of Smad7 in 5/6 nephrectomy rats is less than in normal group. It was higher in RDG groups and Fuxipuli group (P< 0.05). extracellular matrix(ECM) was less in RDG groups and Fuxipuli group. The glomerular sclerosis was less in RDG groups and Fuxipuli group. Conclusion:The Jueyin helm malfunction is the pathological characteristic of CRF, the method of mediating-Jueyin is effective on it. The therapy can adjust transforming growth factor-β1/Smad singaling Pathway (TGF-β1/Smads), remarkably improve the pathological lesion of renal tissue, protect the remaining nephron, retard renal fibrosis.