睾酮对动脉粥样硬化雄兔血凝素样氧化型低密度脂蛋白受体1表达的影响

目的探讨睾酮对动脉粥样硬化雄兔血凝素样氧化型低密度脂蛋白受体1表达的影响。方法选取雄性新西兰白兔18只,随机分为假手术组、去势-安慰剂组和去势-睾酮组,并建立动脉粥样硬化模型。化学发光法测定各组血清总睾酮。胸主动脉HE染色,图像分析测定内膜和中膜厚度。夹心双抗酶联免疫法检测血清氧化型低密度脂蛋白水平。半定量RT-PCR、免疫组织化学分析法测定血凝素样氧化型低密度脂蛋白受体1的mRNA和蛋白表达。结果雄兔去势-安慰剂组血清总睾酮水平显著下降,而去势-睾酮组血清总睾酮水平未见降低,较假手术组差异无显著性。去势-安慰剂组雄兔胸主动脉内膜和内膜/中膜厚度较假手术组显著增加。各组雄兔血清氧化型低密度脂蛋白水平差异无显著性。去势-安慰剂组雄兔胸主动脉血凝素样氧化型低密度脂蛋白受体1的mR-NA和蛋白表达较假手术组显著升高,而去势-睾酮组胸主动脉均无明显改变。结论睾酮对动脉粥样硬化雄兔血清氧化型低密度脂蛋白没有显著影响,但是可影响血凝素样氧化型低密度脂蛋白受体1基因的转录和翻译,睾酮可能通过调节血凝素样氧化型低密度脂蛋白受体1而非氧化型低密度脂蛋白,进而影响动脉粥样硬化的进程。

Effect of Testosterone on Lectin-Like Oxidized Low-Density Lipoprotein Receptor 1 Expression in Atherosclerotic Male Rabbits

AimTo explore whether testosterone plays a role in regulation of lectin-like oxidized low-density lipoprotein receptor 1(LOX-1) in atherosclerotic male rabbits.MethodsThe model of castrated and atherosclerotic male rabbits was prepared.Pathological sections of thoracic aorta were performed hematoxylin-eosin(HE) staining.Total plasma testosterone was measured using ADVIA Centaur Immunoassay(Bayer,Germany) with chemical luminescent method.Serum oxidized low-density lipoprotein(ox-LDL) was assayed using ELISA kit.The expression of LOX-1 of thoracic aorta was measured by methods of RT-PCR,immunohistochemistry.ResultsSerum testosterone significantly decreased in castrated rabbits,whereas testosterone replacement restored the circulating testosterone to normal levels.Intimal thickness and ratio of intima and media obviously increased in castrated rabbits compared with sham-operation rabbits.The serum ox-LDL wasn’t significantly different between each animal.The expression of LOX-1 of thoracic aorta in mRNA and protein was significantly increased in castrated rabbits compared with those in sham-operation rabbits,and decreased in the castrated rabbits following testosterone replacement.ConclusionsTestosterone has no effect on serum ox-LDL in atherosclerotic rabbits,but plays key roles in the mRNA and protein expression of LOX-1 of thoracic aorta.Testosterone possibly regulates the development of athesclerosis via mediating LOX-1 but not ox-LDL.