吉非罗齐对高脂血症鼠一氧化氮活性及血管内皮粘附的影响
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Impact of Gemfibrozil on Nitric Oxide Activity and Cell Adherence of Hyperlipidemic Rats
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    探讨高脂血症在动脉硬化早期对内皮功能的损伤机制。实验分为对照组、高脂血症组和吉非罗齐治疗组,对照组只喂基础饲料,另两组通过4周建立高脂血症模型,此后继续高脂喂养,其中吉非罗齐治疗组在高脂喂养同时喂服吉非罗齐60mg(kg·d),16周后检测三组的总胆固醇、甘油三酯、一氧化氮浓度以及观察血管内皮血管细胞粘附分子1的表达水平和细胞粘附密度。结果发现,与对照组比较,高脂血症组一氧化氮水平降低,血管细胞粘附分子1表达强度增强及范围较广,且白细胞粘附数明显增多。与高脂血症组比较,吉非罗齐治疗组血清一氧化氮水平增高、血管细胞粘附分子1表达水平降低和白细胞粘附数减少。结果提示,高脂血症抑制机体一氧化氮活性,并促进血管细胞粘附分子1对血管内皮的损害,而吉非罗齐可通过改善内皮功能阻止动脉硬化的发生

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    Aim To study the impact of hyperlipidemia on endothelial lesion during the early stage of atherosclerosis. Methods The investigation included control, hyperlipidemic and gemfibrozil treated groups. Hyperlipidemic model was set up on the 4 week atherogenic diet, followed by a 16 week treatment in the treated group [gemfibrozil 60 mg/(kg·d)]. Serum TC, TG, NO level were measured. Expressions of VCAM 1 and cell adhesiveness on aortic endothelium were observed and analyzed by computer aided system. Results Compared with the control group, hyperlipidemic rats showed lower level of NO, stronger and more expansive endothelial expression of VCAM 1. Moreover there was an increase in leukocyte accumulation on the endothelial surface. In contrast, in treated group, expression of VCAM 1 as well as leukocyte adhesion were significantly decreased which associated with improvement of endothelial dysfunction. Conclusions NO activity would be inhibited by hyperlipidemia which facilitated the endothelial impairment of VCAM 1. Gemfibrozil could prevent atherogenesis by restoring endothelial function.

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吴峻,孙明,周宏研.吉非罗齐对高脂血症鼠一氧化氮活性及血管内皮粘附的影响[J].中国动脉硬化杂志,2002,10(6):502~504.

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  • 收稿日期:2002-06-12
  • 最后修改日期:2002-11-12
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