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作 者:万朝敏[1] 邓建军[1] 王正荣[2] 高云钦 俞红吉 吴泰相[3]
机构地区:[1]华西医科大学附属第二医院儿科,成都610041 [2]华西医科大学生物医学工程研究室,成都610041 [3]华西医科大学附属第一医院临床流行病学研究室病毒实验室,成都610041
出 处:《生物物理学报》2000年第2期352-357,共6页Acta Biophysica Sinica
基 金:国家自然科学基金;CMB资助!(基金编号39500036)
摘 要:建立了病毒性心肌炎自身免疫损伤的离体心肌细胞模型 ,在此基础上进行心肌细胞的细胞力学特性和心肌细胞收缩蛋白分子—心肌肌凝蛋白的α重链 (α -MHC) ,β重链 (β-MHC)的mRNA表达水平的分析。发现免疫损伤对心肌细胞有明显的损害 ,造成心肌细胞的变性坏死 ,心肌细胞收缩力下降 ,其中免疫损伤的心肌细胞在24小时的心肌收缩力下降比12小时更为明显 ;经分子生物学分析 ,其收缩蛋白分子基因的表达发生了改变 ,在正常心肌细胞α -MHC相对含量为0.1829±0.023,β-MHC为0.0872±0.005 ,而自身免疫损伤心肌细胞α -MHC相对含量为0.0575±0.005 ,β MHC为0.1015±0.001 ,即由α -MHC表达为主转变成 β-MHC表达为主。结果表明 :免疫损伤使心肌细胞收缩蛋白分子表达发生了改变 ,造成心肌细胞收缩力下降。The mechanism of cell-mediated antoimmune response of cardiac myocyte to coxsackievirus B3 was studied by setting up cellular model of cell-mediated autoimmune injuring myocytes after affected by coxsackivevirus B3(CVB3), then cardiac myocyte mechanics were analyzed and gene expression of the myocardial contractile proteins, α-myosin heavy chain (α-MHC), β-myosin heavy chain (β-MHC) were measured. Results showed that cell-mediated autoimmune response to coxsackivevirus B3 led to damage of cultured cardiac myocytes after incubated with the white blood cells infected by CVB3. The myocyte contractility in immune damaged cardiac myocytes was significantly lower than in normal myocytes(P<0.01). The decrease in myocyte contractility at 24 hours after inducing immunized white blood cells was greater than that at 12 hours. The gene expression level of mRNA for the myocardial contractile protein, α-MHC, was significantly lower in cardiac myocytes after culture with inducing immunized white blood cell (0.0575±0.005) than in normal myocytes (0.1829±0.023). However, the mRNA level forβ-MHC was significantly higher (0.1015±0.001) after inducing immunized white blood cell than in normal myocytes(0.0872±0.005).
分 类 号:R542.210.2[医药卫生—心血管疾病]
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