淫羊藿总黄酮对高脂血症大鼠血清NO、MPO的影响

目的探讨淫羊藿总黄酮降脂及改善氧化应激、炎症对内皮功能的损伤机制。方法 35只刚断乳的SD雄性大鼠经高脂喂养12周后,根据体重随机分为淫羊藿总黄酮大剂量组（9只）和淫羊藿总黄酮小剂量组（9只）和高脂组（8只）,干预4周后检测空腹总胆固醇（TG）、三酰甘油（TC）、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）、一氧化氮（NO）、髓过氧化物酶（MPO）并设普食对照组（9只）。结果高脂组TG、TC、MPO较对照组明显升高（P〈0.01）;淫羊藿总黄酮组TG、TC明显下降;模型组血清NO明显低于对照组和淫羊藿总黄酮组（P〈0.05或P〈0.01）。血清MPO水平淫羊藿总黄酮组较模型组明显下降（P〈0.01）。淫羊藿总黄酮大剂量组较小剂量组下降明显（P〈0.05）。结论血清NO和MPO可能介入高脂饮食氧化应激损伤血管内皮。淫羊藿总黄酮能够从一定程度上改善高脂饮食造成的氧化应激增加所致的内皮损伤,该作用可能通过提高NO水平,降低MPO相关。

Influence of Total Flavonoids of Epimedium on Serum NO and MPO in Rats with Hyperlipidemia

Objective To investigate the effects and mechanisms of total flavonoids of epimedium（TFE） on improvement of hyperlipidemia,inflammation and oxidative stress in functional impairment of the endothelium.Methods Thirty-five SD male rats were randomly divided into four groups：Control group（n=9） fed with normal diet for sixteen weeks,hyperlipidemia group（n=8） fed with high-cholesterol diet for sixteen weeks,TFE low dose group（n=9） and TFE high dose group（n=9） fed with high-cholesterol diet for sixteen weeks supplemented with TFE from the twelveth weeks of cholesterol diet.Serum levels of triglyceride（TG）,total cholesterol（TC）,high density lipoprotein cholesterol（HDL-C）,low density lipoprotein cholesterol（LDL-C）,nitric oxide（NO） and myeloperoxidase（MPO） were detected.Results Compared with control,the serum levels of TG,TC,MPO were increased significantly in hyperlipidemia group（P〈0.01）.Compared with hyperlipidemia group,the serum levels of TG,TC were decreased in TFE group.The contents of serum NO in hyperlipidemia group were higher than that in control group and TFE group（P〈0.05 or P〈0.01）.Compared with hyperlipidemia group,the serum levels of MPO were decreased in TFE group（P〈0.01）.The levels of TFE high dose group were lower than that of TFE low dose group（P〈0.05）.Conclusion NO defeciency and the increase of MPO could be involved in vascular endothelium impairment with oxidative stress in rats with high-fat diet-induce hyperlipidmia,and TFE could ameliorate vascular endothelium impairment by up-regulating NO concentration and down-regulating MPO concentration in rats.