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Attenuation of oxidative stress and cardioprotective effects of zinc supplementation in experimental diabetic rats

机译:糖尿病实验大鼠补锌对氧化应激的减弱和心脏保护作用

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Oxidative stress plays a major role in the pathogenesis of diabetes mellitus, which further exacerbates damage of cardiac, hepatic and other tissues. We have recently reported that Zn supplementation beneficially modulates hyperglycaemia and hypoinsulinaemia, with attendant reduction of associated metabolic abnormalities in diabetic rats. The present study assessed the potential of Zn supplementation in modulating oxidative stress and cardioprotective effects in diabetic rats. Diabetes was induced in Wistar rats with streptozotocin, and groups of diabetic rats were treated with 5- and 10-fold dietary Zn interventions (0.19 and 0.38 g Zn/kg diet) for 6 weeks. The markers of oxidative stress, antioxidant enzyme activities and concentrations of antioxidant molecules, lipid profile, and expressions of fibrosis and pro-apoptotic factors in the cardiac tissue were particularly assessed. Supplemental Zn showed significant attenuation of diabetes-induced oxidative stress in terms of altered antioxidant enzyme activities and increased the concentrations of antioxidant molecules. Hypercholesterolaemia and hyperlipidaemia were also significantly countered by Zn supplementation. Along with attenuated oxidative stress, Zn supplementation also showed significant cardioprotective effects by altering the mRNA expressions of fibrosis and pro-apoptotic factors (by >50 ). The expression of lipid oxidative marker 4-hydroxy-2-nonenal (4-HNE) protein in cardiac tissue of diabetic animals was rectified (68 ) by Zn supplementation. Elevated cardiac and hepatic markers in circulation and pathological abnormalities in cardiac and hepatic tissue architecture of diabetic animals were ameliorated by dietary Zn intervention. The present study indicates that Zn supplementation can attenuate diabetes-induced oxidative stress in circulation as well as in cardiac and hepatic tissues.
机译:氧化应激在糖尿病的发病机制中起主要作用,进一步加剧了心脏、肝脏和其他组织的损伤。我们最近报道了锌补充剂有益地调节高血糖和低胰岛素血症,同时减少糖尿病大鼠的相关代谢异常。本研究评估了补充锌在调节糖尿病大鼠氧化应激和心脏保护作用方面的潜力。用链脲佐菌素诱导Wistar大鼠糖尿病,糖尿病大鼠组接受5倍和10倍膳食锌干预(0.19和0.38g Zn/kg饮食)治疗6周。特别评估了氧化应激、抗氧化酶活性和抗氧化分子浓度、脂质谱以及心脏组织中纤维化和促凋亡因子的表达的标志物。补充锌在改变抗氧化酶活性方面显示出糖尿病诱导的氧化应激显着减弱,并增加了抗氧化分子的浓度。高胆固醇血症和高脂血症也可通过补充锌得到显著缓解。除了减弱氧化应激外,补充锌还通过改变纤维化和促凋亡因子的mRNA表达(>50%)显示出显着的心脏保护作用。补充锌可纠正糖尿病动物心脏组织中脂质氧化标志物4-羟基-2-壬烯醛(4-HNE)蛋白的表达(68 %)。通过饮食锌干预,改善了糖尿病动物循环中心脏和肝脏标志物的升高以及心脏和肝脏组织结构的病理异常。本研究表明,补充锌可以减轻糖尿病引起的循环以及心脏和肝脏组织中的氧化应激。

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