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Anti-oxidant effects of resveratrol on mice with DSS-induced ulcerative colitis.

机译:白藜芦醇对DSS诱导的溃疡性结肠炎小鼠的抗氧化作用。

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BACKGROUND AND AIMS: Oxidant/antioxidant balance is suggested to be an important factor for the recurrence and progression of ulcerative colitis (UC). The aim of the study is to investigate the potential protective role of resveratrol (Res) against dextran sodium sulfate (DSS)-induced oxidative damage in colon of mice with UC. METHODS: UC was induced in mice by oral administration of synthetic DSS (molecular weight 5000) for 7 days. Mice were divided into normal group, colitis control group, low-dose Res-treated group (RLD-treated group), and high-dose Res-treated group (RHD-treated group). Inhibitory effects of concomitant treatment with Res were assessed daily using a Disease Activity Index (DAI) and severity of histological changes. MDA, MPO, SOD and GSH-PX activity of colonic tissue were determined in colon samples by chemical colorimetry. TNF-alpha, IL-8, IFN-gamma, p22(phox) and gp91(phox) expression levels were detected using quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR), ELISA, and Western blot analysis. RESULT: Administration of Res significantly inhibited the severity of UC compared to the colitis control group. Colonic tissue MDA and MPO activities decreased significantly in Res-treated groups compared to colitis control groups. Furthermore, colonic tissue SOD and GSH-Px activities increased significantly in Res-treated groups compared to colitis control groups. The expression levels of TNF-alpha, IL-8, IFN-gamma, p22(phox), and gp91(phox) also decreased significantly in the Res-treated group compared to the colitis control group. CONCLUSIONS: Oral administration of Res exerts marked inhibitory effects on UC in mice. Resveratrol may play an important role in preventing DSS-induced oxidative damage.
机译:背景与目的:氧化剂/抗氧化剂的平衡被认为是溃疡性结肠炎(UC)复发和发展的重要因素。这项研究的目的是调查白藜芦醇(Res)对右旋糖酐硫酸钠(DSS)诱导的UC小鼠结肠氧化损伤的潜在保护作用。方法:口服合成DSS(分子量5000)7天,诱导小鼠UC。将小鼠分为正常组,结肠炎对照组,低剂量Res治疗组(RLD治疗组)和高剂量Res治疗组(RHD治疗组)。每天使用疾病活动指数(DAI)和组织学变化的严重程度评估Res伴随治疗的抑制作用。通过化学比色法测定结肠样品中结肠组织的MDA,MPO,SOD和GSH-PX活性。使用定量逆转录酶聚合酶链反应(qRT-PCR),ELISA和Western blot分析检测TNF-α,IL-8,IFN-γ,p22(phox)和gp91(phox)的表达水平。结果:与结肠炎对照组相比,Res的给药显着抑制了UC的严重程度。与结肠炎对照组相比,Res治疗组的结肠组织MDA和MPO活性显着降低。此外,与结肠炎对照组相比,Res治疗组的结肠组织SOD和GSH-Px活性显着增加。与结肠炎对照组相比,Res治疗组的TNF-α,IL-8,IFN-γ,p22(phox)和gp91(phox)的表达水平也显着降低。结论:口服Res对小鼠的UC有明显的抑制作用。白藜芦醇可能在防止DSS引起的氧化损伤中起重要作用。

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