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目的:探讨血管内皮生长因子(VEGF)预防血管成形术后再狭窄的机制。方法:用高脂饲养建立实验性动脉粥样硬化家兔模型,将VEGF作用于正常健康兔和动脉粥样硬化家兔主动脉血管内皮细胞(VEC)。采用亚硝酸还原法测一氧化氮(NO),放免法测内皮素(ET)、6-酮-前列腺素1α(6-keto-PGF1α),采用发色底物显色法测定血浆纤溶酶原激活物(t-PA)和纤溶酶原激活物抑制物-1(PAI-1)活性。并用WST-1比色法观察VEGF对上述VEC增殖的影响。结果:与空白对照组(VEGF 0μg/L)比较,10μg/L、20μg/L VEGF处理组NO、6-keto-PGF1α、PAI均明显增加,而ET、t-PA、t-PA/PAI均明显降低,并呈剂量依赖性。与正常健康兔VEC(正常VEC)比较,动脉粥样硬化家兔VEC(异常VEC)分泌ET、PAI、t-PA均明显增加,而NO、6-keto-PGF1α、t-PA/PAI均明显降低。结论:动脉粥样硬化家兔伴有内皮功能异常,而VEGF能促进正常和异常VEC的增殖并分泌NO、PGI2、PAI,而抑制ET、t-PA的分泌,使t-PA/PAI降低。
Objective: To investigate the mechanism of vascular endothelial growth factor (VEGF) in preventing restenosis after angioplasty. Methods: Rabbit models of experimental atherosclerosis were established by high fat diet and VEGF was administered to aortic endothelial cells (VECs) of normal rabbits and atherosclerotic rabbits. Nitric oxide (NO) was measured by nitrous acid reduction method and endothelin (ET) and 6-keto-PGF1α were determined by radioimmunoassay. Plasma plasminogen (T-PA) and plasminogen activator inhibitor-1 (PAI-1) activity. The effect of VEGF on the above VEC proliferation was observed by WST-1 colorimetry. Results: NO, 6-keto-PGF1α and PAI in 10μg / L and 20μg / L VEGF groups were significantly increased compared with those in blank control group (0μg / L VEGF) Significantly reduced, and in a dose-dependent manner. The levels of ET, PAI and t-PA were significantly increased in atherosclerotic rabbits compared with those in normal healthy rabbits (normal VEC), while NO, 6-keto-PGF1α and t-PA / PAI were significantly increased reduce. CONCLUSION: Endothelial dysfunction is associated with atherosclerotic rabbits. VEGF can promote the proliferation of normal and abnormal VECs and secrete NO, PGI2 and PAI, but inhibit the secretion of ET and t-PA, leading to the decrease of t-PA / PAI.