Effects of Yishenbupi (tonifying-kidney and invigorating-spleen) prescription on the expression of renal fibrosis-associated proteins in unilateral ureteral occlusion rats

摘要

Objective:To evaluate the effects and mechanism of the Yishenbupi(tonifying-kidney and invigorating-spleen)prescription on the expression of renal fibrosis-associated vimentin,α-SMA,and fibronectin in unilateral ureteral occlusion rats.Methods:A total of 48 SD(Sprague-Dawley)rats were randomly divided into the model,sham-operated(sham),irbesartan,and Yishenbupi groups,with 12 rats in each group.After the unilateral ureteral occlusion model was established,rats in the model and sham groups were administered normal saline,whereas rats in the Yishenbupi group were administered Yishenbupi prescription(18 g/kg/d)intragastrically and those in the irbesartan group were administered irbesartan(10 mg/kg/d)intragastrically.All rats were sacrificed 21 days later.Pathological changes in rat renal tissue were evaluated by H&E staining.The expression of vimentin,α-SMA,and fibronectin in renal tissues was detected by western blotting.Results:Compared with the sham group the model group had renal tubular epithelial cell atrophy,inflammatory cell infiltration accompanied with the proliferation of interstitial collagen fibers,fewer glomeruli,or glomerulosclerosis.Compared with the model group,significantly less renal tubular and glomerular damages,inflammatory cell infiltration,and collagen fibers were observed in different intervention groups,especially in the Yishenbupi group.Compared with the sham group,significantly higher expressions of fibrosis markers,including vimentin,α-SMA,and fibronectin,were observed in the model group.Compared with the model group,the expression of anti-fibrosis markers,including vimentin,α-SMA and fibronectin,was significantly decreased in both the irbesartan and Yishenbupi groups(P<0.01);however,the Yishenbupi group showed higher efficacy than the irbesartan group(P<0.05).Conclusion:The Yishenbupi prescription may improve renal fibrosis by reducing the expression of fibrosis-associated vimentin,α-SMA,and fibronectin.