| Objective:To discuss the protective and its possible mechanism of Shendibushen Capsule on adriamycin-induced focal segmental glomerular sclerosis (FSGS) rats, To investigate morphological changes in the kidney and renal functions, from the promotingã€anti fibrosis cell factors and matrix metalloproteinases and tissue inhibitor of metalloproteinase aspects, to illustrate the mechanism of Shendibushen Capsule on delaying chronic renal failure and inhibit glomerular sclerosis.Methods:The FSGS rat model was induced by nephrectomy of left kidney plus intravenous injection of adriamycin. The general state of the rats were observed before and after treatment, the 24h urinary protein and the changes of serum BUNNã€Scrã€ALBã€Cholã€TG were observed. HE and Masson staining method for renal pathologic slice were used to observe the pathological changes of the experimental rats kidney tissue after treatment, Immunohistochemical method was performed on renal tissue to detect the expression of TGF-β1ã€CTGFã€PDGF-BBã€HGFã€BMP-7ã€MMP-9ã€TIMP-1, Reverse transcriptase Polymerase Chain Reaction(RT-PCR) was used to detect the expression of TGF-β1mRNA and TIMP-1mRNA in each group of rats kidney tissue.Results:The physical status and symptom of the glomerular sclerosis rats were improved obviously after treating by Shendibushen Capsule, reduce 24 h urinary protein and BUNã€Scr in blood serum, elevate serum albumin level, regulate blood lipid, reduce the pathlological changes which has the significant difference compared with control groups, shendibushen Capsule can reduce the expression of TGF-β1ã€CTGFã€PDGF-BBã€TIMP-1 and promote the expression of HGFã€BMP-7ã€MMP-9, which has the significant difference compared with control groups, The expression of TGF-β1mRNA and TIMP-1mRNA were also reducedConclusions:The shendibushen Capsule can decrease the 24 h urinary protein, reduce BUNã€Scr in blood serum, elevate serum albumin level,regulate blood lipid,improve the renal function;reduce glomerular sclerosis index, protect the renal ultra structure; inhibit the expression of fibrogenic factor TGF-β1ã€CTGFã€PDGF-BB, reduce ECM synthesis; increase the expression of anti fibrosis factor HGFã€BMP-7, promote the degradation of ECM; regulate The main degradation system ECM(MMPs/TIMPs), promote the expression of MMP-9,reduce the expression of TIMP-1,To maintain the balance of synthesis and degradation of ECM,then reduce the degree of glomerular sclerosis; reduce the expression TGF-β1mRNA and TIMP-1mRNA, Therefore, the progression of glomerular sclerosis was delayed. |