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目的通过观察环氧化酶Ⅱ(cyclooxygenase-2,COX-2)、诱导型前列腺素合成酶Ⅰ(membrane associatedprostaglandin E-1,mPGES-1)在兔动脉粥样硬化(AS)斑块中的表达水平及阿伐他汀对其的干预作用。方法取40只体质量为2.0～2.2 kg的3月龄健康雄性新西兰兔,随机分为正常对照组8只(普通饲料);高脂模型组32只(高胆固醇饲料)。8周后将高脂模型组再分为模型组、阿伐他汀治疗Ⅰ组、Ⅱ组及Ⅲ组[剂量分别为2.5、5及10 mg/(kg.d),n=8]。6周后取各组兔冠状动脉,检测其COX-2及mPGES-1的表达;同时,采血检测各组血清总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)及极低密度脂蛋白胆固醇(VLDL-C)浓度。结果模型组血清TC、TG、HDL-C、LDL-C及VLDL-C水平与正常对照组比较差异显著(P<0.05);而阿伐他汀治疗Ⅱ组及Ⅲ组上述各项指标与模型组比较差异显著(P<0.05);阿伐他汀治疗Ⅰ组各项血脂水平较之模型组无显著差异(P>0.05)。与正常对照组比较,模型组动脉粥样硬化组织的COX-2及mPGES-1表达显著增高(P<0.05);与模型组比较,治疗Ⅱ组、Ⅲ组动脉粥样硬化组织的COX-2及mPGES-1表达明显下调(P<0.05)。结论阿伐他汀可能通过降低COX-2/mPGES-1表达、降低血脂,进而发挥其对AS的治疗作用。
Objective To investigate the expression of cyclooxygenase-2 (COX-2) and membrane associatedprostaglandin E-1 (mPGES-1) in atherosclerotic plaques of rabbits Level and the role of atorvastatin on it. Methods Forty three-month-old healthy male New Zealand white rabbits weighing 2.0-2.2 kg were randomly divided into normal control group (n = 8) and high-fat model group (n = 32) After 8 weeks, the model group was subdivided into model group and atorvastatin group Ⅰ, Ⅱ and Ⅲ [dosage was 2.5, 5 and 10 mg / (kg · d), n = 8]. After 6 weeks, the coronary arteries of rabbits in each group were taken out to detect the expression of COX-2 and mPGES-1. At the same time, the levels of total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol C), low density lipoprotein cholesterol (LDL-C) and very low density lipoprotein cholesterol (VLDL-C) concentrations. Results The levels of TC, TG, HDL-C, LDL-C and VLDL-C in the model group were significantly different from those in the normal control group (P <0.05) (P <0.05). There was no significant difference in serum lipids between atorvastatin group and model group (P> 0.05). Compared with the normal control group, the expression of COX-2 and mPGES-1 in atherosclerotic tissue in the model group was significantly increased (P <0.05). Compared with the model group, the COX-2 And mPGES-1 expression was significantly down-regulated (P <0.05). Conclusions Atorvastatin may reduce the level of lipids by decreasing the expression of COX-2 / mPGES-1, and then exert its therapeutic effect on AS.