中文摘要：

目的观察辛伐他汀对动脉粥样硬化（As）大鼠高迁移率族蛋白B1（HMGBI）表达及斑块形态学的影响，以期揭示其抗AS的作用机制。方法60只Wistar大鼠按随机数字表法均分为对照组、AS模型组、辛伐他汀干预组。给予高脂饮食同时灌胃维生素D3建立AS模型；干预组于第8周开始给予辛伐他汀2．5mg·kg-1·d-1灌胃；各组分别于10周、12周用免疫组化法检测主动脉粥样硬化斑块内HMGBl蛋白表达，实时逆转录一聚合酶链反应（RT—PCR）检测HMGB1mRNA表达，并观察主动脉斑块形态学变化。结果模型组主动脉斑块内HMGB1蛋白表达呈强阳性，辛伐他汀干预组HMGB1表达较模型组明显减少，12周时更为显著。与对照组比较，模型组10周、12周时HMGBlmRNA表达均明显升高（10周：19．695±1．418、比2．981±0．753，12周：20．542±1．132比3．219±0．332，均P〈0．01）；辛伐他汀干预组10周、12周HMGB1mRNA表达（15．798±0．891，12．641±0．734）明显低于模型组相应时间点，且12周时表达低于10周时（P〈0．05或P〈0．01）。模型组主动脉内有明显钙化斑块，呈环状，斑块遍及整条动脉；辛伐他汀干预后可明显抑制斑块形成，12周斑块面积较10周时进一步减小。结论辛伐他汀能减轻AS大鼠主动脉粥样斑块形成，降低斑块组织中HMGB1的蛋白及mRNA表达，通过减轻炎症反应起到血管保护作用。

英文摘要：

Objective To observe the effect of simvastatin on the expression of high mobility group box-1 protein （HMGB1） and morphology of atherosclerotic plaques in atherosclerotic rats, to ascertain whether HMGB1 plays a role in the preventive mechanism of simvastatin from atherosclerosis （AS）. Methods Sixty Wistar rats were divided randomly into three groups： control group, model group and simvastatin treatment group. Gastric gavage of vitamin D3 with high fat food was used to reproduce atherosclerotic rat model. The rats in the treatment group were treated with simvastatin of 2.5 mg· kg 1 · d-1 （gatric perfusion） 8 weeks after fat diet. The expression of the histopathology and protein of HMGB1 in atheroselerotic plaques of the aorta was observed by immunohistochemistry at 10 weeks and 12 weeks. The gene expression of HMGB1 at atherosclerotic plaques of aorta was observed with real time-polymerase chain reaction （RT-PCR）. The morphology of the atherosclerotic plaques was observed. Results The expression of HMGB1 increased significantly in atherosclerotie plaques in model group, and simvastatin could evidently inhibit the expression of HMGB1, and it was more obvious in 12-week group. Compared with control group, the HMGB1 mRNA expression was upregulated in all atherosclerotic model groups （10 weeks：19. 695± 1. 418 vs. 2. 981±0. 753, 12 weeks.. 20. 542±1. 132 vs. 3. 219±0. 332, both P〈0.01）. In the simvastatin treatment group, the. gene expression of HMGB1 was lower than the age-match model group at 10 weeks （15. 798±0. 891） and 12 weeks （12. 641±0. 734）, and in the 12-week treatment group it was lower than that in the 10-week treatment group （P〈0.05 or P〈0.01）. In the model group, the ring-shape calcified atherosclerotic plaques were extensively found in the wall of the aorta. Simvastatin could obviously inhibit the formation of the atherosclerotic plaques, and the effect was more obvious in the 12-week treatment group than that of the 10-week treatment group. Conclusion