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维生素 E 和胡颓子提取物可降低尼古丁诱导的大鼠心脏氧化应激。

Vitamin E and Hippophea rhamnoides L. extract reduce nicotine-induced oxidative stress in rat heart.

机构信息

Department of Physiology, Ataturk University, Erzurum, Turkey.

出版信息

Cell Biochem Funct. 2010 Jun;28(4):329-33. doi: 10.1002/cbf.1663.

Abstract

The effects of vitamin E and Hippophea rhamnoides L. extract (HRe-1) on nicotine-induced oxidative stress in rat heart were investigated. There were eight rats per group and supplementation period was 3 weeks. The groups were: nicotine [0.5 mg kg(-1)day(-1), intraperitoneal (i.p.)]; nicotine plus vitamin E [75 mg kg(-1)day(-1), intragastric (i.g.)]; nicotine plus HRe-1 (250 mg kg(-1)day(-1), i.g.); and the control group (receiving only vehicles). Nicotine increased the malondialdehyde level, which was prevented by both vitamin E and HRe-1. Glutathione peroxidase (GPx) activity in nicotine plus vitamin E supplemented group was higher than the others. Glutathione S-transferase (GST) activity in nicotine plus HRe-1 supplemented group was increased compared with the control group. Catalase activity was higher in nicotine group compared with others. GPx activity in nicotine plus vitamin E supplemented group was elevated compared with the others. Total and non-enzymatic superoxide scavenger activities in nicotine plus vitamin E supplemented group were lower than nicotine plus HRe-1 supplemented group. Superoxide dismutase (SOD) activity was higher in nicotine plus HRe-1 supplemented group compared with others. Glutathione reductase activity and nitric oxide level were not affected. Increased SOD and GST activities might have taken part in the prevention of nicotine-induced oxidative stress in HRe-1 supplemented group in rat heart. Flavonols such as quercetin, and isorahmnetin, tocopherols such as alpha-tocopherol and beta-tocopherol and carotenoids such as alpha-carotene and beta-carotene, reported to be present in H. rhamnoides L. extracts may be responsible for the antioxidant effects of this plant extract.

摘要

研究了维生素 E 和沙棘提取物(HRe-1)对尼古丁诱导的大鼠心脏氧化应激的影响。每组 8 只大鼠,补充期为 3 周。各组分别为:尼古丁[0.5mgkg(-1)day(-1),腹腔内(i.p.)];尼古丁加维生素 E[75mgkg(-1)day(-1),灌胃(i.g.)];尼古丁加 HRe-1(250mgkg(-1)day(-1),灌胃);对照组(仅给予载体)。尼古丁增加了丙二醛水平,这一水平被维生素 E 和 HRe-1 共同阻止。尼古丁加维生素 E 补充组的谷胱甘肽过氧化物酶(GPx)活性高于其他组。与对照组相比,尼古丁加 HRe-1 补充组的谷胱甘肽 S-转移酶(GST)活性增加。与其他组相比,尼古丁组的过氧化氢酶活性更高。与其他组相比,尼古丁加维生素 E 补充组的 GPx 活性升高。尼古丁加维生素 E 补充组的总和非酶超氧化物清除活性低于尼古丁加 HRe-1 补充组。与其他组相比,尼古丁加 HRe-1 补充组的超氧化物歧化酶(SOD)活性升高。谷胱甘肽还原酶活性和一氧化氮水平不受影响。SOD 和 GST 活性的增加可能参与了 HRe-1 补充组对尼古丁诱导的大鼠心脏氧化应激的预防。黄酮醇如槲皮素、异槲皮素、生育酚如α-生育酚和β-生育酚以及类胡萝卜素如α-胡萝卜素和β-胡萝卜素,据报道存在于沙棘提取物中,可能是这种植物提取物具有抗氧化作用的原因。

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