非诺贝特对高甘油三酯血症患者血管内皮的保护作用及机制探讨
非诺贝特,,非诺贝特;过氧化物酶体增生物激活受体;高甘油三酯血症;肿瘤坏死因子;丙二醛;一氧化氮,1材料与方法,2结果,3讨论,【参考文
【摘要】 目的 研究显示非诺贝特可改善高脂血症患者血管内皮功能,这种作用主要归功于其调脂作用。近年来其调脂外作用是研究的热点。本实验旨在探讨在高甘油三酯血症的患者,非诺贝特是否可通过抗氧化和抗炎症作用诱导类似的血管内皮保护作用。方法 本试验选择健康对照20例和单纯高甘油三酯血症患者24例,后者接受非诺贝特(200mg/d)治疗8周,观察治疗前后血管内皮依赖性舒张功能(FMD)的变化,以及血清中血脂水平、NO、丙二醛(MDA)、肿瘤坏死因子(TNF-α)的变化。结果 与对照组相比,高甘油三酯血症患者血管内皮依赖性舒张功能明显下降,NO生成减少,MDA、TNF-α水平明显升高,非诺贝特治疗8周后明显改善血管内皮依赖性舒张功能,增加NO的生成,降低MDA、TNF-α水平。结论 结果提示非诺贝特诱导的血管内皮保护作用与激动PPARα受体调脂、抗氧化和抗感染反应有关。【关键词】 非诺贝特;过氧化物酶体增生物激活受体;高甘油三酯血症;肿瘤坏死因子;丙二醛;一氧化氮
Effect of fenofibrate on endothelial function in hypertriglyceridemic patients
XIA Da, LI Shu, WU Xian-ming. Department of Cardiology, Yiyang Municipal Central Hospital, Yiyang 413000,China
【Abstract】 Objective Studies have demonstrated that fenofibrate, a ligand of peroxisome proliferator-activated receptor-α (PPARα), attenuated the impairment of endothelial function in hyperlipidemic individuals. Although the beneficial effects of fenofibrate were primarily attributed to its lipid-regulating effects, much attention was paid to its no-lipid-regulating actions. Methods 20 healthy controls and 24 hypertriglyceridemic subjects to receive fenofibrate treatment (200mg/d)were mecruited in the present study. Serum levels of nitric oxide (NO), malondialdehyde (MDA) and tumor necrosis factor-α(TNF-α) were measured. Endothelial function assessed by flow-mediated dilation (FMD) of the brachial artery was performed. Results Compared with control, serum levels of MDA and TNF-α were markedly elevated, and the level of NO was significantly reduced, concomitantly with impaired endothelium-dependent vasodilation in individuals with hypertriglyceridemia. 8-week treatment with fenofibrate significantly reduced the elevated levels of MDA and TNF-α, attenuated the decreased level of NO and improved endothelial function. Conclusions These results suggest that the beneficial effect of fenofibrate on the endothelium in hypertriglyceridemic individuals may be related to lipid-regulating effect, antioxidant and anti-inflammatory actions via activating PPARα receptor. ......
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