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机构地区:[1]复旦大学附属华山医院老年病科,上海200040
出 处:《中国现代医学杂志》2016年第17期1-6,共6页China Journal of Modern Medicine
基 金:上海市卫生和计划生育委员会科研基金项目(No:20134459)
摘 要:目的探讨茶多酚对代谢综合征(MS)大鼠糖脂代谢的干预作用及其分子作用机制。方法高糖高脂饮食诱导建立MS大鼠模型,经茶多酚干预16周后测定各组大鼠血脂、血糖、空腹胰岛素及游离脂肪酸水平,计算胰岛素抵抗指数。逆转录聚合酶链反应法检测各组大鼠脂肪组织过氧化物酶体增殖剂激活受体-γ、脂联素、肿瘤坏死因子-α、磷脂酰肌醇3-激酶、蛋白激酶B的m RNA表达,Western blot法检测大鼠脂肪组织上述细胞因子在蛋白水平的表达。结果茶多酚干预组大鼠血三酰甘油、胆固醇、低密度脂蛋白、空腹血糖、游离脂肪酸水平均较MS对照组下降(P<0.05),经茶多酚干预后MS大鼠胰岛素抵抗指数较对照组下降(P<0.05)。干预组脂肪组织过氧化物酶体增殖剂激活受体-γ、脂联素、磷脂酰肌醇3-激酶、蛋白激酶B的m RNA及蛋白表达水平较代谢综合征对照组均有上调(P<0.05),药物干预组肿瘤坏死因子-α的m RNA及蛋白表达水平较MS对照组下调(P<0.05)。结论茶多酚可以通过降低游离脂肪酸水平及肿瘤坏死因子-α的表达,增加过氧化物酶体增殖剂激活受体-γ、蛋白激酶B、磷脂酰肌醇3-激酶、脂联素的表达来改善MS大鼠的糖脂代谢。Objective To observe the effect of tea polyphenols on rats with metabolic syndrome (MS) and its molecular mechanism. Methods A rat model of metabolic syndrome was induced by high-glucose and high-fat diet. After intervention of tea polyphenols for 16 weeks the levels of blood glucose, blood fat, fasting insulin and free fatty acid were detected, and the index of insulin resistance (HOMA-IR) was calculated. The mRNA expressions of peroxisome proliferators activiated receptor-Y (PPAR-Y), adiponectin, TNF-a, phos- phatidylinositol-3 kinase (PI3K) and protein kinase B in adipose tissue were detected by RT-PCR; and their protein expressions were detected by Western blot. Results The levels of fasting blood glucose, triglyceride, cholesterol, LDL, free fatty acid and HOMR-IR in the tea polyphenol group were significantly lower than those in the control group (P〈 0.05). Compared with the control group, the mRNA and protein expressions of PPAR-Y, adiponectin, PI3K and protein kinase B in the adipose tissue of the tea polyphenol group were up- regulated (P 〈 0.05). The mRNA and protein expressions of TNF-a in the tea polyphenol group were signifi- cantly lower than those in the control group (P 〈 0.05). Conclusions Tea polyphenols can improve glucolipid metabolism in MS rats through decreasing the levels of free fatty acid and TNF-a while increasing the ex- pressions of PPARY protein kinase B, PI3K and adiponectin.
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