阿司匹林抗动脉粥样硬化作用及机制

Effects and mechanism of aspirin on the experimental atherosclerosis

目的观察阿司匹林对大鼠动脉粥样硬化(AS)的预防性干预作用,并探讨阿司匹林抗AS的作用及其可能的作用机制。方法采用高脂饮食方法建立大鼠AS模型。放射免疫法检测血脂;通过荧光分光光度计检测胸主动脉和腹主动脉组织内糖基化终产物(AGEs)的含量;采用定量病理学测量大鼠主动脉斑块面积、内膜面积、斑块面积/内膜面积比、血管周长;光学显微镜下观察主动脉壁粥样硬化的改变。结果模型组(model)的血脂检测、AGEs含量、形态学及病理学与普通饲料喂养组比较差异有统计学意义(P<0.05),证实造模成功。阿司匹林高低剂量组(AH组、AL组)与模型组的总胆固醇差异无统计学意义(P>0.05);AL组的主动脉组织内AGEs含量较模型组显著降低(P<0.05);AL、AH组均可见散在的斑块生长、血管内膜光滑,与模型组比较,AL组、AH组间的斑块面积、斑块面积/内膜面积变化不大(P>0.05),但有下降趋势。光学显微镜下观察:模型组主动脉内膜结构不完整、中膜明显钙化、胶原增生;AL组、AH组主动脉内皮结构完整,中膜钙化程度较模型组减轻。结论阿司匹林不影响大鼠的血脂水平,但可减轻血管壁钙化,延缓AS斑块的形成。

Objective To investigate the anti-atherosclerosis effects of aspirin and its action mechanism through animal models of experimental atherosclerosis. Methods Experimental atherosclerosis models of rats were made by feeding them with high fat diet. The blood fat of all the rats was detected by radioimmunity method. The quantity of advanced glycation end products （AGEs） in thoracic aorta and abdominal aorta was measured by fluorospectrophotometer. The area of the plaque and endomembrane, the perimeter of aorta and the ratio of plaque endomembrane in the area were measured by quantitative pathology. The atherosclerotic changes of the aorta were observed by optical microscope. Results Hyperlipemia models and atherosclerosis models of rats were confirmed by pathological examination and blood fat detection. There was no significant difference in blood fat between AH, AL group and model group（P〉0.05）. The AGEs content in AL group was significantly lower than that in model group（P〈0.05）;the aorta endomembrane in AL group and AH group was smooth,with sporadic plaque. The area of plaque and the ratio of plaque /endomembrane were not significantly decreased in AL, AH group, as compared with those in model group（P〉0.05） , however the tendency of decrease was found. The examination results of optical microscope showed that the integrated aorta endothelial structure was not found in model group, however,the calcified tunica media with proliferation of collagen was found. Both AL group and AH group had integrated aorta endothelial structure, and the calcification of tunic media, which were lighter than those in model group. Conclusion Aspirin doesn＇ t affect the levels of blood fat in experimental atherosclerosis models of rats. But it can relieve the calcification of aorta and can delay the genesis of atherosclerosis plaque.