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Objective:To investigate the possible protective effect and mechanism of ginsenoside Rb1 against oxidative damage and renal interstitial fibrosis on rats with unilateral ureteral obstruction(UUO). Methods:In total,80 male rats were randomly divided into 4 groups,20 in each group:the sham operated group (SOR),UUO group,UUO with ginsenoside Rb1 treatment group(treated with intraperitoneal injection of 50 mg/ kg daily) and UUO with Losartan treatment group(as the positive control,treated with 20 mg/kg by gastrogavage per day).The rats were randomly sacrificed on day 3,7 and 14 after surgery,respectively.The histopathologic changes of renal interstitial tissues were observed with Masson staining.The mRNA of transforming growth factorβ1(TGF-β1),collagenⅠand fibronectin were reversed transcribed and quantified by Real-time PCR.Enzyme-linked immunosorbent assay was used to quantitatively detect TGF-β1 and 8-hydroxy-2’-deoxyguanosine (8-OHdG) levels.P47phox protein expression was assessed by immunohistochemistry and Western blot analysis.Results:In the UUO model,the obstructed kidney showed typical features of progressive renal tubulointerstitial fibrosis,and the levels of TGF-β1,collagenⅠand fibronectin increased(P<0.05).As compared with the UUO group,ginsennoside Rb1 significantly inhibited the interstitial fibrosis including tubular injury and collagen deposition,and decreased the levels of TGF-β1(P<0.05).Ginsenoside Rb1 also inhibited the heme oxygenase(HO-1) and 8-OHdG,two markers of oxidative stress(P<0.05).Moreover,ginsenoside Rb1 suppressed the expression of p47phox,a subunit of nicotinamide adeninedinucleotide phosphate(NADPH) oxidase(P<0.05).Conclusion:Ginsenoside Rb1 can obviously inhibit renal interstitial fibrosis in rats with UUO, its mechanism possibly via against the oxidative damage and suppressing TGF-β1 expression.
Method:In total,80 male rats were randomly divided into 4 groups,20 in each group: Objective:To investigate the possible protective effect and mechanism of ginsenoside Rb1 against oxidative damage and renal interstitial fibrosis on rats with unilateral ureteral obstruction(UUO). The sham operated group (SOR), UUO group, UUO with ginsenoside Rb1 treatment group (treated with intraperitoneal injection of 50 mg/ kg daily) and UUO with Losartan treatment group (as the positive control, treated with 20 mg/kg by gastrogavage per ())The rats were arranged sacrificed on day 3,7 and 14 after surgery,respectively.The histopathologic changes of renal interstitial models was observed with Masson staining.The mRNA of transforming growth factorβ1(TGF-β1),collagen I and fibronectin were reversed transcribed And quantified by Real-time PCR.Enzyme-linked immunosorbent assay was used to quantitatively detect TGF-β1 and 8-hydroxy-2’-deoxyguanosine (8-OHdG) levels.P47phox protein expression was assessed. By immunohistochemistry and Western blot analysis.Results:In the UUO model,the obstructed children showed typical features of progressive renal tubulointerstitial fibrosis,and the levels of TGF-β1,collagenIand fibronectin increased (P<0.05).As compared with the UUO group, Ginsennoside Rb1 significantly inhibited the interstitial fibrosis including tubular injury and collagen deposition, and decreased the levels of TGF-β1 (P<0.05). Ginsenoside Rb1 also inhibited the heme oxygenase (HO-1) and 8-OHdG, two markers of oxidative stress (P<0.05). Moreover, ginsenoside Rb1 suppressed the expression of p47phox, a subunit of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (P<0.05). Conclusion: Ginsenoside Rb1 can significantly inhibit renal interstitial fibrosis in rats with UUO, its mechanism possibly Via against the oxidative damage and suppressing TGF-β1 expression.