GINSENOSIDE RB1,A PANOXADIOL SAPONIN AGAINST OXIDATIVE DAMAGE AND RENAL INTERSTITIAL FIBROSIS IN RATS WITH UNILATERAL URETERAL OBSTRUCTION

• 来源期刊: 中国结合医学杂志(英文版)
• 学科: 医学
• 关键词: 山口
• 年，卷（期）: 2009,（2）
• 页码范围: 133-140
• 页数: 8页
• 分类号: R285.5
• 语种: 中文

摘要

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.