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目的:研究阿托伐他汀对家兔颈动脉粥样硬化(AS)斑块内巨噬细胞及平滑肌肌动蛋白(SMA)表达的影响,并探讨他汀类药物稳定AS斑块的机制。方法:24只健康雄性新西兰大耳白兔随机分为对照组(n=8)和高胆固醇血症组(n=16)。16只高胆固血症组的家兔喂饲高胆固醇饲料2周后,进行颈总动脉内膜球囊拉伤术,术后再随机等分为AS模型组和阿托伐他汀组[给予阿托伐他汀5 mg/(kg.d)],两组均继续喂饲高胆固醇饲料10周。喂养第12周时处死动物,取颈总动脉进行石蜡切片,用酶标法检测不同时间点血清脂质和脂蛋白;应用光学显微镜观察AS的进程;采用免疫组化染色法检测巨噬细胞浸润和SMA在斑块处的表达。结果:阿托伐他汀组的血清总胆固醇(TC)及低密度脂蛋白-胆固醇(LDL-C)的浓度明显低于AS模型组(P<0.01),颈总动脉内膜的厚度较AS模型组显著变薄[(0.49±0.072)vs.(0.66±0.08)mm,P<0.05]。免疫组化染色法检测结果示,阿托伐他汀组血管壁中巨噬细胞的数量显著较模型组减少(P<0.05)而SMA的表达较AS模型组显著增多(P<0.01)。结论:阿托伐他汀可能通过抑制AS斑块内巨噬细胞的浸润并增强SMA的表达,而发挥稳定斑块的作用。
Objective: To investigate the effect of atorvastatin on the expression of macrophages and smooth muscle actin (SMA) in rabbits with carotid atherosclerosis (AS) plaque and to explore the mechanism of stabilizing AS plaque in statins. Methods: Twenty-four healthy male New Zealand white rabbits were randomly divided into control group (n = 8) and hypercholesterolemia group (n = 16). Sixteen hypercholesterolaemic rabbits were fed with hypercholesterolemia for 2 weeks, then carotid artery endarterectomy balloon injury was performed and then randomly divided into AS model group and atorvastatin group [given Atorvastatin 5 mg / (kg · d)], two groups were fed high cholesterol diet for 10 weeks. Animals were sacrificed on the 12th week, paraffin sections of the common carotid artery were taken, and serum lipids and lipoproteins were detected by enzyme-linked immunosorbent assay (ELISA) at different time points. The course of AS was observed with light microscope. The infiltration of macrophages And SMA expression at the plaque. Results: The levels of total cholesterol (TC) and low density lipoprotein cholesterol (LDL-C) in atorvastatin group were significantly lower than those in AS model group (P <0.01) Group was significantly thinner [(0.49 ± 0.072) vs. (0.66 ± 0.08) mm, P <0.05]. The results of immunohistochemical staining showed that the number of macrophages in the atorvastatin group was significantly decreased compared with the model group (P <0.05), while the expression of SMA was significantly increased in the atorvastatin group compared with the AS model group (P <0.01). Conclusion: Atorvastatin may play a role in stabilizing plaque by inhibiting the infiltration of macrophages in AS plaque and enhancing the expression of SMA.