扩张型心肌病大鼠肿瘤坏死因子α及基质金属蛋白酶1的表达  

Expression of tumor necrosis factor-α and matrix metalloproteinase-1 in rats with dilated cardiomyopathy

作　　者：黄荣杰[1] 刘唐威 庞玉生[3] 

机构地区：[1]广西医科大学第二医院ICU,广西南宁530007 [2]广西心血管病研究所,广西南宁530022 [3]广西医科大学第一医院儿科,广西南宁530022

出　　处：《基础医学与临床》2005年第5期424-428,共5页Basic and Clinical Medicine

基　　金：广西科学科技攻关项目(科攻关0322025-7)

摘　　要：目的探讨扩张型心肌病对大鼠左心室肌肿瘤坏死因子α(TNF-α)和基质金属蛋白酶1(MMP1)表达水平的影响及与二者的关系.方法用呋喃唑酮饲养大鼠4～8周,超声心动图检测大鼠左心室结构和功能,HE和VG染色分别观察大鼠心肌细胞和间质胶原纤维的变化,RT-PCR检测左室心肌MMP1 mRNA的表达水平,免疫组化检测左室心肌组织TNF-α和MMP1表达水平.结果扩张型心肌病的大鼠左心室增大,收缩功能下降;心肌细胞肥大、变性,间质纤维明显增生;左室心肌组织TNF-α和MMP1表达水平上调.结论扩张型心肌病的大鼠左室肌TNF-α和MMP1的表达水平上调,两者在心肌纤维化及左室重构中起重要作用;TNF-α等细胞因子的激活伴有MMP1表达上调.Objective To explore the expression of tumor necrosis factor (TNF)-α and matrix metalloproteinase-1(MMP1) and their relationship in the rats with dilated cardiomyopathy. MethodsThe Wistar rat model of dilated cardiomyopathy was created by feeding with furazolidone for 48 weeks. Myocardial cell morphology was observed by HE stain. The protein of tumor necrosis factor (TNF)-α and matrix metalloproteinase-1 were detected by immunochemistry, and the mRNA gene expression was detected via reverse transcription-polymerase chain reation (RT-PCR). ResultsIn the rat with dilated cardiomyopathy, the left ventricular interior diameter was increased and cardiac funtion decreased, cardiac myocyte hypertrophy and lysis accompanied with nucleus augmentation and differentiation, and the expression of TNF-α and MMP1 was upgraded. ConclusionThe expression of TNF-α and MMP1 upregulation plays a main role in myocardum fibrisis and left ventricular remodeling in rats with furazolidone-induced dilated cardiomyopathy. The cytokine activation such as TNF-α be one of the mechanisms of MMP1 upregulation.

关 键 词：扩张型心肌病 基质金属蛋白酶1 大鼠 肿瘤坏死因子α(TNF-α) RT-PCR检测 左室心肌组织 超声心动图检测 MMP1 免疫组化检测 心肌细胞肥大 结构和功能 左心室增大 心肌纤维化 左心室肌 呋喃唑酮 胶原纤维 mRNA 收缩功能 

分 类 号：R542.2[医药卫生—心血管疾病] R394.8[医药卫生—内科学]