论文部分内容阅读
目的观察慢性缺氧对兔血浆中磷脂酶A2(PLA2)、脂蛋白相关PLA2(Lp-PLA2)和溶血磷脂酸(LPA)水平及促动脉粥样硬化的影响。方法将12只健康新西兰白兔随机分为正常对照组和慢性缺氧组(建立慢性缺氧动物模型),每组6只。分别在实验前、实验第4周、8周和12周末取外周血,应用ELISA法检测各组兔血浆中PLA2、Lp-PLA2和LPA水平,并于12周末取各组兔主动脉弓和腹主动脉进行超声检测和HE染色,观察血管病理改变。结果与正常对照组和同组实验前比较,慢性缺氧组兔第4、8和12周末,血浆中PLA2、Lp-PLA2和LPA水平不同程度增高,且在12周时增高最明显(P<0.05)。在12周时,与正常对照组比较,慢性缺氧组兔主动脉弓及腹主动脉的血管壁上均有不同程度的动脉粥样硬化形成。结论慢性缺氧能上调兔血浆中PLA2、Lp-PLA2和LPA水平,增加动脉粥样硬化形成,在促动脉粥样硬化的形成中发挥重要作用。
Objective To observe the effect of chronic hypoxia on plasma PLA2, Lp-PLA2, LPA and atherosclerosis in rabbits. Methods Twelve healthy New Zealand white rabbits were randomly divided into normal control group and chronic hypoxia group (chronic hypoxia model), 6 in each group. The levels of PLA2, Lp-PLA2 and LPA were measured by ELISA before and after the experiment at the 4th, 8th and 12th week respectively. At the end of the 12th week, the aortic arch and the abdominal aorta Ultrasonic examination and HE staining were performed to observe the vascular pathological changes. Results Compared with the normal control group and the control group before the experiment, the levels of PLA2, Lp-PLA2 and LPA in the plasma of the chronic hypoxia group increased to the highest extent at the 4th, 8th and 12th week, and increased most significantly at the 12th week (P < 0.05). At 12 weeks, compared with the normal control group, the aortic arch and the abdominal aortic wall in chronic hypoxia group had different degrees of atherosclerosis. Conclusion Chronic hypoxia can up-regulate the levels of PLA2, Lp-PLA2 and LPA in rabbit plasma and increase the formation of atherosclerosis, which play an important role in the development of atherosclerosis.