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目的 探讨对氧磷酶在脑梗死发病机理中的作用 ,其活性改变与脑梗死患者脂质过氧化状态的关系。方法 测定了 39名脑梗死患者与 2 1名年龄相匹配的健康体检者血清对氧磷酶 (PON1)活性、血脂水平、氧化型低密度脂蛋白 (OX LDL)含量、丙二醛 (MDA)水平及超氧化物歧化酶 (SOD)活力。结果 脑梗死组血清PON1活性较对照组明显降低 (95 .94± 4 3.97VS 137.6 9± 5 1.81,P <0 .0 1)、甘油三脂 (TG)、低密度脂蛋白 (LDL)、载脂蛋白B(apoB)较对照组升高 (分别是P <0 .0 1,P <0 .0 1,P <0 .0 5 ) ,OX LDL明显升高 (P <0 .0 1) ,同时SOD活力明显下降 (P <0 .0 1) ,而MDA水平则显著增加 (P <0 .0 1)。结论 在脑梗死发病机理中 ,脂质代谢紊乱、血清PON1活性降低等因素促使脂质过氧化的发生 ,引起动脉粥样硬化。脑缺血、缺氧又进一步促发自由基的链式反应 ,引起脑细胞膜的脂质过氧化损伤 ,导致脑梗死的发生。
Objective To investigate the role of paraoxonase in the pathogenesis of cerebral infarction and its relationship with the changes of lipid peroxidation in patients with cerebral infarction. Methods Serum levels of plasma paraoxonase (PON1), serum lipids, oxidized low density lipoprotein (OX LDL), malondialdehyde (MDA) and serum levels of PON1 were measured in 39 patients with cerebral infarction Level and superoxide dismutase (SOD) activity. Results The serum PON1 activity of cerebral infarction group was significantly lower than that of the control group (95.94 ± 4.97 vs 137.6 9 ± 5 1.81, P <0.01), triglyceride (TG), low density lipoprotein (LDL) Compared with the control group, the level of apoB increased (P <0.01, P <0.01, P <0.05) At the same time, SOD activity decreased significantly (P <0.01), but MDA level increased significantly (P <0.01). Conclusion In the pathogenesis of cerebral infarction, lipid metabolism disorders, serum PON1 activity decreased and other factors promote the occurrence of lipid peroxidation, causing atherosclerosis. Cerebral ischemia, hypoxia and further promote the free radical chain reaction, causing lipid peroxidation of brain cell membrane damage, leading to the occurrence of cerebral infarction.