于熙滢, 曹海利, 刘雅君, 刘洋, 李晓光, 班翔, 魏林. 阿托伐他汀对家兔颈动脉粥样硬化斑块内巨噬细胞浸润和平滑肌肌动蛋白表达的影响[J]. 心脏杂志, 2011, 23(1): 46-50.
    引用本文: 于熙滢, 曹海利, 刘雅君, 刘洋, 李晓光, 班翔, 魏林. 阿托伐他汀对家兔颈动脉粥样硬化斑块内巨噬细胞浸润和平滑肌肌动蛋白表达的影响[J]. 心脏杂志, 2011, 23(1): 46-50.
    Effect of atorvastatin on expression of macrophage and smooth muscle actin in carotid atherosclerotic plaques in rabbits[J]. Chinese Heart Journal, 2011, 23(1): 46-50.
    Citation: Effect of atorvastatin on expression of macrophage and smooth muscle actin in carotid atherosclerotic plaques in rabbits[J]. Chinese Heart Journal, 2011, 23(1): 46-50.

    阿托伐他汀对家兔颈动脉粥样硬化斑块内巨噬细胞浸润和平滑肌肌动蛋白表达的影响

    Effect of atorvastatin on expression of macrophage and smooth muscle actin in carotid atherosclerotic plaques in rabbits

    • 摘要: 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。

       

      Abstract: AIM: To observe inflammatory macrophages and smooth muscle actin in carotid atherosclerotic plaques in rabbits and the effects of atorvastatin on them and to explore whether statins could stabilize carotid plaques and its possible mechanism. METHODS: Twenty-four rabbits were randomly divided into three groups: control group (n=8) and hypercholesterolemia group (n=16). The hypercholesterolemia group was fed a hypercholesterol diet for 2 weeks and then catheter-induced arterial wall injury was made. Rabbits in hypercholesterolemia and aortic injury group were randomized into model group (n=8) and atorvastatin group 5 mg/(kg·day) for 10 weeks (n=8). Carotid arteries were isolated and paraffin-embedded slices were obtained. Blood lipids and lipoproteins were detected and the development of atherosclerotic plaques was evaluated by light microscopy. The levels of macrophages and smooth muscle actin in the common carotid artery were measured by immunohistochemical analysis. RESULTS: Serum concentrations of TC and LDL-C in atorvastatin group were lower than those in hypercholesterolemia model group (P<0.01). The intimal-medial thickness [(0.49±0.072)mm vs.(0.66±0.079)mm, P<0.05] in atorvastatin group was significantly less than that in hypercholesterolemia model group. Immunohistochemical analysis showed much less stain in macrophages in atorvastatin group compared with that in hypercholesterolemia model group. More smooth muscle actin was observed in atherosclerotic plaque than that in atorvastatin group. CONCLUSIONS: Atorvastatin may decrease the level of macrophages in atherosclerotic plaque and increase the development of smooth muscle actin, thus prohibiting the formation and development of atherosclerosis.

       

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