Objective:RIF is the common pathway of progressive renal disease to the end stage renal failure. A large number of studies demonstrated that the degree of TIF was correlated with the degree of decline in renal function and prognosis of renal disease, the more serious TIF was,the faster renal function declined and the worse the prognosis of kidney disease became. So, more and more people attached importance to TIF. The pathogenesis of TIF was a very complex process of chronic pathology,During which, inflammatory cell infiltration、avariety of cells releasing many inflammatory cytokines、myofibroblasts differentiated from tubular epithelial cells and mesenchymal cells had very important roles. However, so far the effective reliable treatment of anti-TIF was absent clinically. PNS was mainly active ingredient extracted from traditional herb Panax notoginseng ,which had many biological effects including the strong role of anti-fibrotic tissues and organs. Past studies showed that PNS could inhibit inflammatory cells、inflammatory factors in tubulointerstitial、myofibroblasts differentiated from tubular epithelial cells and mesenchymal cells and improve renal microcirculation etc. Much progress about the studies of PNS interfering TIF had been made in recent years,However,which focused on the treatment after TIF formation. The studies of TIF early interfered were very less. The main purpose of this study aimed to observe the role of PNS in the prevention and treatment of adenine nephropathy rat model at the early stage, explore its possible mechanism and also provide a theoretical basis for PNS clinically interfering TIF .Methods:Fifty male clearly healthy Wister rats were randomly divided into 3 groups: normal group(n=6),adenine treated group(n=22) and PNS treated group(n=22). Tubulointerstitial fibrosis models were established by gavage with 250 mg.kg~(-1).d~(-1) adenine solved in a solution of 2 % starch for 21d. After 7d, PNS 50 mg.kg~(-1).d~(-1) was injested into the abdomens of the rats in PNS treated group. On days 7,14,21 and 28,Concentration of platelet-derived growth factor (PDGF) -BB in serum was determined by enzyme linked immunosorbent assay (ELISA) methods, 24 h Urine protein content was determined by huangliusuan methods, the rat kidneys were examed pathologically by HE,Masson staining and immunohistochemmical staining forα–smooth muscle action (α–SMA) expression,meanwhile,semiquantitative analysis was performed.Results:On days 7d、14d、21d and 28d,the level of serum PDGF–BB in PNS treated group and adenine treated group was higher than in normal group(P < 0.05),which in PNS treated group was lower than in adenine treated group on days 14d、21d and 28d(P < 0.05); On days 7d、14d、21d and 28d,24 h Urine protein content in PNS treated group and adenine treated group was higher than in normal group(P < 0.05),which in PNS treated group was lower than in adenine treated group on days 21d and 28d(P < 0.05); Masson staining showed that on days 7d、14d、21d and 28d, semiquantitative analysis for TIF in PNS treated group and adenine treated group was higher than in normal group(P < 0.05),which in PNS treated group was lower than in adenine treated group on days 21d and 28d ( P < 0.05 ) ; Immunohistochemmical staining demonstrated that on days 7d、14d、21d and 28d, semiquantitative analysis forα–SMA expression was higher than in normal group(P < 0.05),which in PNS treated group was lower than in adenine treated group on days 21d and 28d(P < 0.05); HE staining showed that inflammatory cell infiltration、the renal interstitial edema、the renal tubular expansion and the renal tubular atrophy were reduced in PNS treated group at the same time point ,in contrast to adenine treated group.Conclusions:PNS might inhibit tubulointerstitial fibrosis in adenine nephropathy rat model at the early stage by suppressing the level of PDGF-BB in serum、reducing 24 h Urine protein content and the expression ofα–SMA in the tubulointerstitium. PNS might reduce inflammatory cell infiltration、the renal interstitial edema、the renal tubular expansion and the renal tubular atrophy and slow down the progress of renal interstitial fibrosis.