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Resveratrol protects against oxidative stress by activating the Keap-1/Nrf2 antioxidant defense system in obese-asthmatic rats

机译:通过在肥胖的哮喘大鼠中激活Keap-1 / NRF2抗氧化防御系统来保护氧化应激免受氧化应激

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The aim of the present study was to investigate the potential mechanism underlying the anti-obesity-asthmatic effects of resveratrol (RSV) in a rat model of obese-asthma. Rat models of obesity and asthma were established using a high-fat diet and the administration of ovalbumin, respectively. Rats were divided into 7 different groups: A normal control, a normal obese, a normal asthma, a normal obese + asthma, a RSV obese, a RSV asthma and a RSV obese + asthma group. Body weight, Lee index, body fat and lung histopathological changes were evaluated. Serum lipid levels were evaluated using calorimetric methods. Levels of reactive oxygen species (ROS) were examined using enzyme-linked immunosorbent assays. Cellular antioxidant enzyme activities were measured using commercial kits. Levels of kelch-like ECH associated protein 1 (Keap-1) and nuclear factor erythroid 2-related factor 2 (Nrf2) was examined using western blot analysis. The results indicated that obese and asthma rat models were successfully established. It was also demonstrated that RSV decreased fasting blood glucose in obese, asthmatic and obese-asthmatic rats. RSV altered serum lipid levels; it significantly increased high density lipoprotein cholesterol levels and significantly decreased serum triglyceride, serum total cholesterol and very low density lipoprotein levels, compared with untreated obese, asthmatic and obese-asthmatic rats (P0.05). ROS levels were significantly decreased in the RSV treatment group compared with obese, asthmatic and obese-asthmatic rats (P0.05). RSV treatment significantly increased catalase, glutathione, glutathione peroxidase and total superoxide dismutase levels compared with untreated obese, asthmatic and obese-asthmatic rats (P0.05). Furthermore, RSV treatment significantly downregulated Keap-1 and upregulated Nrf2 levels in the heart, lung and kidney tissues of rats compared with untreated controls. Therefore, the results demonstrate that RSV protects against oxidative stress by activating the Keap-1/Nrf2 antioxidant defense system in obese-asthmatic rat models.
机译:本研究的目的是研究白藜芦醇(RSV)在肥胖哮喘大鼠模型中的抗肥胖性哮喘效应的潜在机制。使用高脂肪饮食和卵磷蛋白分别建立了肥胖和哮喘的大鼠肥胖和哮喘模型。大鼠分为7种不同的组:正常对照,正常肥胖,正常的哮喘,正常的肥胖+哮喘,RSV肥胖,RSV哮喘和RSV肥胖+哮喘组。评估体重,李指数,体脂和肺组织病理学变化。使用量温方法评估血清脂质水平。使用酶联免疫吸附试验检查反应性氧物质(ROS)的水平。使用商业试剂盒测量细胞抗氧化酶活性。使用蛋白质印迹分析检查蛋白质样蛋白和核因子红外蛋白1(Keap-1)和核因子红细胞2相关因子2(NRF2)。结果表明,成功建立了肥胖和哮喘大鼠模型。还表明RSV减少了肥胖,哮喘和肥胖的哮喘大鼠的空腹血糖。 RSV改变血清脂质水平;与未处理的肥胖,哮喘和肥胖的哮喘大鼠相比,它显着提高了高密度脂蛋白胆固醇水平,并且显着降低了血清甘油三酯,血清甘油三酯,血清总胆固醇和非常低密度的脂蛋白水平(P <0.05)。与肥胖,哮喘和肥胖的哮喘大鼠相比,RSV治疗组中ROS水平显着降低(P <0.05)。与未处理的肥胖,哮喘和肥胖的哮喘大鼠相比,RSV治疗显着增加了过氧化氢酶,谷胱甘肽,谷胱甘肽过氧化物酶和总超氧化物歧化酶水平(P <0.05)。此外,与未处理的对照相比,RSV治疗显着下调Keap-1和大鼠肾和肾组织的上调NRF2水平。因此,结果表明RSV通过在肥胖的大鼠模型中激活Keap-1 / NRF2抗氧化防御系统来保护氧化应激。

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