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机构地区:[1]青岛大学医学院医学营养研究所,青岛266021 [2]青岛大学医学院附属医院,青岛266071
出 处:《营养学报》2009年第6期574-578,共5页Acta Nutrimenta Sinica
基 金:山东省科技厅(No2006GG2302002)
摘 要:目的观察凹顶藻萜类化合物(Laurencia terpenoids extract,LTE)对酒精暴露大鼠的抗氧化水平及HO-1酶活性的影响,并探讨其可能的作用机制。方法60只雄性Wistar大鼠随机分为6组。酒精模型组(B组)给予乙醇4.8g/kgbw·d灌胃;LTE低、中、高剂量干预组(C、D、E组)分别给予LTE25、50、100mg/kgbw·d;甘利欣药物组(F组)给予甘利欣200mg/kgbw·d灌胃。空白对照组(A组)给予等体积蒸馏水。除空白组外,酒精剂量均同模型组。实验进行6w。分别测定血清及肝匀浆中超氧化物歧化酶(SOD)和谷胱甘肽过氧物酶(GSH-Px)活性,丙二醛(MDA)含量。对肝组织切片进行免疫组化染色,观察肝内血红素氧化酶-1(HO-1)免疫阳性细胞的组织分布,并对其灰度值和光吸收密度值进行定量分析。结果与A组比,B、F组血清及肝匀浆SOD活力下降,C、E组血清SOD活力比B组升高,有一定的量效关系。B组大鼠血清及肝匀浆GSH-Px活力较A组下降,而D组较B组显著升高。与A组比,B组血清及肝匀浆MDA含量较A组升高,而D、E组血清和肝匀浆MDA含量较B组显著降低,且有一定的量效关系。与A组比,B组HO-1活力显著降低。D、E、F组HO-1活力比B组升高明显。结论LTE可增强酒精暴露大鼠体内抗氧化的活性,减少脂质过氧化产物的生成,诱导HO-1活性增强,从而对酒精造成的机体氧化损伤表现出相应的保护效应。Objective To study the preventive effect of Laurencia terpenoids extract(LTE)on antioxidant system after alcohol exposure in rats. Method Sixty male Wistar rats were randomly assigned to six groups: Group A (blank group) was ig distilled water. Group B (model group) drink 50% alcohol of 4.8g/kg bw·d. Group C, D and E was ig supplemented with LTE of 25, 50 and 100 mg/kg bw·d respectively. Group F (positive contro1) was fed diammonium glycyrrhizinate 200 mg/kg bw·d. All rats were treated for 6w. Six weeks later, the blood and hepatic tissue were collected. The activities of superoxide dismutase (SOD), glutathione-peroxidase (GSH-Px), the content of malonaldehyde (MDA) in plasma were measured by biochemical methods. The expression of heme oxygenase-1 (HO-1) in hepatic tissue was measured by immunohistochemistry assay. Results Compared with blank group, the activities of SOD and GSH-Px in serum and hepatic tissue decreased; but the contents of MDA in serum and hepatic tissue of B group increased. Compared with model group, the activities of SOD in serum of C,D,E groups increased; and the activities of GSH-Px in serum and hepatic tissue of C,D, F groups increased; but the contents of MDA in serum and hepatic tissue of C,D,E groups decreased. HO-1 was expressed in liver cells surrounding central veins of hepatic lobules. Compared with blank group, the expression of HO-1 in B group was decreased. Compared with model group, the expression of HO-1 in D,E,F groups was increased. Conclusion LTE can protect against oxidant injury after alcohol exposure, which may be associated with increased activity of antioxidant enzymes, reduced lipid peroxidation, and increased expression of HO-1 in liver cells.
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