小鼠病毒性心肌损伤过程中炎症介质表达异常及其组织学改变的研究  

Abnormal Expression of Inflammatory Mediators and Pathological Alteration of Myocardial Injury in Mice during Coxsackievirus B3 Infection

作　　者：高增栋[1] 朱健华[1] 姚登福[1] 吴玮[1] 张彬[1] 施公胜[2] 刘春[1] 

机构地区：[1]南通医学院附属医院心内科,南通226001 [2]南通医学院实验动物中心

出　　处：《南通医学院学报》2004年第2期127-129,132,共4页ACTA Academiae Medicinae Nantong

基　　金：江苏省自然科学基金资助项目 ( NO:BK99160 )

摘　　要：目的 :研究小鼠柯萨奇病毒 B3感染过程中炎症介质动态表达与心肌组织损伤间的关系。方法 :于Balb/ c小鼠腹腔接种 1× 10 8TCID50 柯萨奇病毒 B3(CVB3)液 ,诱发心肌损伤的发生 ,在 CVB3感染后观察 2 1天 ,分别在第 3、6、9、12、15、18和 2 1天 ,采集外周血作肿瘤坏死因子 (TNF-α)和一氧化氮合酶 (NOS)分析 ,并留取心肌组织进行病理组织学观察。结果 :对照组心肌无改变 ,实验组小鼠心肌细胞出现肿胀 ,横纹不清 ,胞质染色嗜酸性增强 ,胞核出现核固缩及核碎裂、变性、坏死崩解 ,胞核和细胞轮廓消失 ,周围出现炎性细胞浸润 (主要是单核细胞和淋巴细胞 ) ,间质内可见较多的胶原纤维 ,可见钙化灶 ;超微结构的电镜观察 ,可见线粒体肿胀、嵴断裂、严重空泡样变及细胞核异形变、染色质浓缩边聚。在病毒感染过程中 ,NOS和 TNF-α异常升高并呈动态的双峰型改变 ,第 2峰与心肌的损伤密切相关。结论 :柯萨奇病毒 B3感染引起心肌细胞损伤 ,可能与炎症介质。Objective:To observe the relationship between dynamic expression of inflammatory mediators and myocardial injury after coxsackievirus B3 (CVB3) infection.Methods:Viral myocardial injury models in BALB/c mice were created by intraperitoneal inoculation with CVB3(1×10 8 TCID) to induce occurrence of mice myocardial injury. The mice were sacrificed at the 3rd, 6th, 9th, 12th, 15th, 18th, and 21st day after the virus infection; hearts were reserved to do pathological examination by conventional histologic staining methods.Results:The myocardial pathological examination demonstrated that no changes took place in the control mice,and in the CVB3-infected mice,salient histopathologic features were present, including myocardial swelling, unclear and strong acidophil staining, pyknosis, karyorrhexis, karyolysis, cell outline disappearance,inflammatory cell infiltration (most of mono nucleus cells and lymphocytes), calcification and fibrination by staining with Hematoxylin and Eosin.Mitochondrial swelling and rupture, severity vacancy-like denatureation and nucleus abnormality,condensed chromatin borders were found under electron microscope in microstructure of cardiac myocytes. The dynamic alterations of NOS and TNF-αlevels showed two peaks after virus inoculation, The first was significantly associated with increased inflammatory response, and the second was closely related with mice myocardial injury.Conclusions:The present data suggested that coxsackievirus B3 infection resulted in mice myocardial injury, and inflammatory mediators and cytokines participated in the process of disease.

关 键 词：柯萨奇病毒B3 心肌细胞 损伤 炎症介质 小鼠 

分 类 号：R363.2[医药卫生—病理学]