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热量限制对乙醇诱导的氧化性和硝化性心脏毒性及大鼠血浆脂质的影响。

The effects of caloric restriction against ethanol-induced oxidative and nitrosative cardiotoxicity and plasma lipids in rats.

机构信息

Institute of Pathophysiology, "Ljubodrag Buba Mihailović", Faculty of Medicine, University of Belgrade, Belgrade 11000, Serbia.

出版信息

Exp Biol Med (Maywood). 2013 Dec;238(12):1396-405. doi: 10.1177/1535370213506806. Epub 2013 Oct 24.

Abstract

Caloric restriction (CR) prevents or delays a wide range of aging-related diseases possibly through alleviation of oxidative stress. The aim of our study was to examine the effect of CR on oxidative and nitrosative cardiac damage in rats, induced by acute ethanol intoxication. Male Wistar rats were divided into following groups: control; calorie-restricted groups with intake of 60-70% (CR60-70) and 40-50% of daily energy needs (CR40-50); ethanol-treated group (E); calorie-restricted, ethanol-treated groups (CR60-70 + E, CR40-50 + E). Ethanol was administered in five doses of 2 g/kg every 12 h, while the duration of CR was five weeks before ethanol treatment. Malondialdehyde level was significantly lower in CR60-70 + E and significantly higher in CR40-50 + E vs. control. Nitrite and nitrate level was significantly higher in CR40-50 + E compared to control group. Activity of total superoxide dismutase (SOD) and its isoenzyme, copper/zinc-SOD (Cu/ZnSOD), was significantly higher in CR60-70 + E and lower in CR40-50 + E vs. control. Activity of manganese-SOD (MnSOD), that is also SOD isoenzyme, was significantly lower in  CR40-50 + E compared to control group. Plasma content of sulfhydryl (SH) groups was significantly higher in CR60-70 group vs. control. Plasma concentration of total cholesterol, triacylglycerol, low-density lipoproteins and high-density lipoproteins was significantly lower in CR60-70 group compared to control values. Food restriction to 60-70% of daily energy needs has a protective effect on acute ethanol-induced oxidative and nitrosative cardiac damage, at least partly due to alleviation of ethanol-induced decrease in SOD activity, while restriction to 40-50% of energy needs aggravates lipid peroxidation and nitrosative stress.

摘要

热量限制(CR)通过减轻氧化应激,预防或延缓多种与衰老相关的疾病。我们的研究目的是观察 CR 对急性乙醇中毒诱导的大鼠心脏氧化和硝化损伤的影响。雄性 Wistar 大鼠分为以下几组:对照组;热量限制组,能量摄入为每日需求量的 60-70%(CR60-70)和 40-50%(CR40-50);乙醇处理组(E);热量限制,乙醇处理组(CR60-70+E、CR40-50+E)。乙醇以 2g/kg 的 5 个剂量每 12 小时给药一次,而 CR 持续时间为乙醇处理前 5 周。与对照组相比,CR60-70+E 组丙二醛水平显著降低,而 CR40-50+E 组丙二醛水平显著升高。与对照组相比,CR40-50+E 组硝酸盐和亚硝酸盐水平显著升高。总超氧化物歧化酶(SOD)及其同工酶铜/锌-SOD(Cu/ZnSOD)的活性在 CR60-70+E 组显著升高,在 CR40-50+E 组显著降低。Mn-SOD(MnSOD)的活性,也是 SOD 同工酶,在 CR40-50+E 组明显低于对照组。与对照组相比,CR60-70 组血浆巯基(SH)含量显著升高。CR60-70 组的血浆总胆固醇、三酰甘油、低密度脂蛋白和高密度脂蛋白浓度明显低于对照组。

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