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作 者:王建丽[1] 高春荣[2] 李莉[1] 袁中瑞[1] 张晓明[1] 李伯勤[3] 胡维诚[1] S.M.Schwartz
机构地区:[1]山东大学医学院病理与病理生理学研究所 [2]山东大学齐鲁医院 [3]山东大学医学院超微结构室,山东济南250012 [4]Department of Pathology,University of Washington,Seattle,WA,USA
出 处:《中国病理生理杂志》2006年第3期431-434,共4页Chinese Journal of Pathophysiology
基 金:山东省自然科学基金资助项目(No.Y2003C07)
摘 要:目的:探讨动脉外膜炎症诱发载脂蛋白E基因剔除(apoE-/-)小鼠冠状动脉粥样硬化病灶发生的机制。方法:取apoE-/-小鼠心脏做连续切片,选择冠状动脉外膜有炎性细胞浸润的3类部位代表粥样硬化病灶形成过程中的3个阶段:①未发现粥样硬化病灶;②有直接从主动脉延伸的病灶顶端和③成熟粥样硬化病灶的冠状动脉。分别采用HE染色、Movat染色、免疫组化和透射电镜方法鉴定3个病变阶段的冠状动脉外膜中炎细胞类型。结果:①未发现粥样硬化病灶;②有直接从主动脉延伸的病灶顶端和③成熟粥样硬化病灶的冠状动脉外膜分别以巨噬细胞、中性粒细胞和淋巴细胞浸润为主,其构成比分别为60.00%、57.65%和66.67%,各组构成比分别与其它两组比较均有显著差异(P<0.01)。结论:动脉外膜炎症可能是诱发动脉粥样硬化发生的早期事件之一,ApoE-/-小鼠冠状动脉粥样硬化病灶形成过程中,动脉外膜经历了一个从急性炎症到慢性炎症的过程。AIM: To study the pathogenesis of atheresclerotic lesions which were closely related to the advenfifial inflammation of coronary artery (CA) in apolipoprotein E gene knockout ( apoE - / - ) mice. METHODS: The hearts of apoE - / - mice were cut consecutively. Three kinds of CA samples (① Infiltration of inflammatory cells at CA advenfitia, without lesion; ② Infiltration of inflammatory cells at CA adventitia, with the top of extending lesion directly from aorta; ③ Infiltration of inflammatory cells at CA adventitia, with mature lesion) were chosen to represent the three stages of atheresclerotic lesion formation. HE staining, Movat staining, immunohistochemical staining and electron transmission microscopy were used respectively to identify the types of the inflammatory cells infiltrated at adventitia of coronary artery. RESULTS: The constituent ratio of macrophages which infiltrated in the CA adventitia without atheresclerotic lesions, of neutmphils which were involved in the CA adventitia with young atheresclerotic lesions and of lymphocytes in the CA adventitia with mature lesions, were 60.00%, 57.65% and 66.67%, which were higher than those in the other two groups, respectively ( P 〈 0.01 ). CONCLUSION: It was showed that CA adventitial inflammation might be an early event inducing the formation of atheresclemtic lesions. The CA adventitia undergoes a process from acute to chronic inflammation during the formation of atherosclerotic lesions.
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