茶多酚对代谢综合征大鼠血管通透性影响

Effect of green tea polyphenols on vascular hyperpermeability in rats with metabolic syndrome induced by high fat diet

目的探讨绿茶多酚对高脂膳食诱导代谢综合征大鼠血管通透性升高的干预效果。方法雄性wist-ar大鼠随机分为正常对照、高脂对照、茶多酚低、中、高剂量干预组,断乳后开始给予高脂饮食,达到成年体重后进行茶多酚干预,持续30周,测定大鼠体重、脂肪系数、血糖、血脂水平,采用伊文思蓝注射法测定大鼠血管通透性,硝酸根还原酶法测定大鼠血清一氧化氮(NO)水平,采用试剂盒测定内皮型一氧化氮合酶(eNOS)、诱导型一氧化氮合酶(iNOS)活性,制作血管冷冻切片,采用二氢乙啶荧光探针检测其活性氧分子(ROS)水平。结果与对照组(0.16±0.007)μg/mg比较,高脂组大鼠血管通透性(0.19±0.006)μg/mg明显升高,与高脂组比较,低、中、高茶多酚组大鼠血管通透性[(0.16±0.004)、(0.14±0.010)、(0.15±0.010)μg/mg]明显降低;茶多酚组ROS水平明显低于高脂组;与高脂组比较,茶多酚明显上调eNOS活性,而下调iNOS活性。结论绿茶多酚对代谢综合征大鼠血管通透性升高具有保护作用,其保护效应可能与减轻氧化损伤有关。

Objective To study the effect of green tea polyphenols（GTPs） on metabolic syndrome-related vascular hyperpermeability in rats.Methods Male Wistar rats were randomly divided into 5 groups：normal control,high fat diet control,low,moderate,and high dose GTPs（100,200,400 mg/kg · bw · d） treated groups.GTPs intervention were applied when the body weight of the rats were up to 180 g.After 30 weeks,the permeability of aortic artery were measured with Evans blue injection method.The nitric oxide（NO） levels in the serum,the activity of inducible nitric oxide synthase（iNOS） and ehdothelial nitric oxide synthase（eNOS） was measured with commercial kit.The aortic artery of the rats were harvested and frozen slides were prepared.The reactive oxygen species（ROS） levels were tested by dihydroethidium（DHE） fluorescent probe.Results The vascular permeability of the high fat diet group（0.19±0.006 μg/mg） was significantly higher than that of the control group（0.16±0.007 μg/mg）.GTPs treatment downregulated the vascular permeability（0.16±0.004,0.14±0.010,and 0.15±0.010 μg/mg,respectively） compared with that of the high fat diet group.The ROS level in GTPs treated groups was significantly lower than that of high fat diet group.Compared with the high fat diet group,GTPs upregulated eNOS activity and downregulated iNOS activity.Conclusion GTPs treatment has protective effects on metabolic syndrome related vascular hyperpermeability in rats.The mechanism might be related to the alleviation of oxidative damage.