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作 者:钱素娟[1] 于祖熙[2] 于维汉[1] 万汇娟[1] Victor.J.Ferrans
机构地区:[1]哈尔滨医科大学克山病研究所,黑龙江哈尔滨150086 [2]美国国立卫生研究院心,肺,血液研究所病理研究室,美国208921518
出 处:《中国地方病学杂志》2000年第5期327-329,I002,共4页Chinese Jouranl of Endemiology
摘 要:目的 嗜鼠心肌 Coxsackie B3病毒 (CVB3m)可诱导 BAL B/C小鼠病毒性心肌炎 (VMC)。探讨自由基一氧化氮 (NO)与 VMC心肌损伤的关系。方法 给 BAL B/C小鼠腹腔接种 0 .1m l 10 0 TCD5 0 CVB3m,感染后分批断脊处死小鼠。应用双重荧光染色技术、原位末端标记法 (TU NEL )和共聚焦显微镜对小鼠心肌中细胞凋亡、NO相关合成酶 (NOS1 、NOS2 和 NOS3)及其降解产物 (Nitrotyrosine)和肌钙蛋白 (Troponin I,Tn I)的表达进行检测。结果 TU NEL法检测发现 ,感染后 7~ 15 d,小鼠心肌中可见明显的心肌细胞及炎细胞凋亡 ,2 0 d后逐渐减少。感染鼠心肌中 Nitrotyrosine和 NOS2 蛋白表达同时期增加 ,阳性细胞分布区域与脱失 Tn I的细胞分布区域基本一致 ,表达量的动态改变与炎性损伤程度一致。双重荧光染色显示 ,部分 NOS2 阳性炎细胞及心肌细胞同时可见凋亡标记。 NOS1 、NOS3的表达在感染前、后各时间点无明显差异。结论 在 CVB3m诱发的小鼠心肌炎实验中 ,由 NOS2 诱导产生的 NO可直接参与细胞凋亡及心肌细胞变性。Objective This study is to explore the Nitric Oxide involved in the cardiac damages of mice myocaditis induced by CVB 3m .Methods BALB/C mice were inoculated with 0.1ml 100 TCD 50 CVB 3m and batch sacrificed later.Immunohistochemical observations,including TUNEL labeling,single and dual fluorescent labeling techniques,were performed on mice hearts,and the results were detected by a confocal laser scanning microscope.Results The myocarditis was detected from all CVB 3m infected mice and was most severe at 7~12 days.Apoptosis also increased markedly in inflammatory cells and myocytes at 9~15 days after infection.Immunoreactivities for NOS 2 and Nitrotyrosine increased considerably in myocardium after infection,and decreased gradually after 20 days,as inflammation subsided.The distribution of these two signals in myocytes were similar to those seen in the lost of TnI.Double staining for NOS 2 and apoptosis were observed in some inflammatory cells and myocytes.Conclusions Our data suggest that in experimental viral myocarditis in mice,NO,which was induced by NOS 2,take a part in the development of myocarditis by the regulation of apoptosis and the damage of myocardium.
分 类 号:R542.210.2[医药卫生—心血管疾病]
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