国际病毒学杂志
國際病毒學雜誌
국제병독학잡지
INTERNATIONAL JOURNAL OF VIROLOGY
2013年
5期
227-229
,共3页
急性病毒性心肌炎%心肌纤维化%转化生长因子β1%内皮质间充质转化
急性病毒性心肌炎%心肌纖維化%轉化生長因子β1%內皮質間充質轉化
급성병독성심기염%심기섬유화%전화생장인자β1%내피질간충질전화
Acute viral myocarditis%Myocardial fibrosis%Transforming growth factor beta 1%Ectomesenchymal transformation within the cortex
目的 探讨心脏内皮质间充质转化(endothelial to mesenchymal transition,EndMT)与急性病毒性心肌炎纤维化的关系.方法 选取实验室Balb/c小白鼠30只,分为心肌炎组、对照组及重组人骨形成蛋白7 (recombinant human bone morphogenetic protein-7,rh-BMP-7)干预组,每组各10只.用药后7天取小鼠心脏标本,计算心脏胶原容积积分,检测小鼠心脏器官中转化生长因子β1(transforming growth factor-β1,TGF-β1)、成纤维细胞特异性蛋白1(fibroblast specific proteins-1,FSP-1)、内皮细胞标志物、Ⅰ型胶原蛋白(collagen type l,Colαl)和基因以及α-平滑肌肌动蛋白(α-smooth muscle actin,α-SMA)的表达情况.结果 与对照组相比,心肌炎组小鼠坏死心肌呈现明显纤维化,同时出现了内皮细胞表型丢失和EndMT现象.与心肌炎组小鼠相比,干预组EndMT现象和心肌纤维化较轻.结论 TGF-β1为心肌纤维化的主要介导因子,引导EndMT.抵制TGF-β1可抵制心肌纤维化过程.
目的 探討心髒內皮質間充質轉化(endothelial to mesenchymal transition,EndMT)與急性病毒性心肌炎纖維化的關繫.方法 選取實驗室Balb/c小白鼠30隻,分為心肌炎組、對照組及重組人骨形成蛋白7 (recombinant human bone morphogenetic protein-7,rh-BMP-7)榦預組,每組各10隻.用藥後7天取小鼠心髒標本,計算心髒膠原容積積分,檢測小鼠心髒器官中轉化生長因子β1(transforming growth factor-β1,TGF-β1)、成纖維細胞特異性蛋白1(fibroblast specific proteins-1,FSP-1)、內皮細胞標誌物、Ⅰ型膠原蛋白(collagen type l,Colαl)和基因以及α-平滑肌肌動蛋白(α-smooth muscle actin,α-SMA)的錶達情況.結果 與對照組相比,心肌炎組小鼠壞死心肌呈現明顯纖維化,同時齣現瞭內皮細胞錶型丟失和EndMT現象.與心肌炎組小鼠相比,榦預組EndMT現象和心肌纖維化較輕.結論 TGF-β1為心肌纖維化的主要介導因子,引導EndMT.牴製TGF-β1可牴製心肌纖維化過程.
목적 탐토심장내피질간충질전화(endothelial to mesenchymal transition,EndMT)여급성병독성심기염섬유화적관계.방법 선취실험실Balb/c소백서30지,분위심기염조、대조조급중조인골형성단백7 (recombinant human bone morphogenetic protein-7,rh-BMP-7)간예조,매조각10지.용약후7천취소서심장표본,계산심장효원용적적분,검측소서심장기관중전화생장인자β1(transforming growth factor-β1,TGF-β1)、성섬유세포특이성단백1(fibroblast specific proteins-1,FSP-1)、내피세포표지물、Ⅰ형효원단백(collagen type l,Colαl)화기인이급α-평활기기동단백(α-smooth muscle actin,α-SMA)적표체정황.결과 여대조조상비,심기염조소서배사심기정현명현섬유화,동시출현료내피세포표형주실화EndMT현상.여심기염조소서상비,간예조EndMT현상화심기섬유화교경.결론 TGF-β1위심기섬유화적주요개도인자,인도EndMT.저제TGF-β1가저제심기섬유화과정.
Objective To investigate the relationship between endothelial mesenchymal transition and fibrosis of acute viral myocarditis.Methods 30 laboratory mice were chosen.They were divided into three groups including the myocarditis group,the control group,and the recombinant human bone morphogenetic protein-7 (group).The heart specimens of the mice were taken after interference for 7 days.The integral of cardiac collagen volume was calculated.The expression in mice heart about transforming growth factor-β1,fibroblast specific proteins-1,collagen type 1 and α-smooth muscle actin were inspected.Results Compare with the comparison team,the necrosis of myocardium of the mice in myocarditis group has an obvious tendency of fibrosis.Compare with the myocarditis team,the recombinant human bone morphogenetic protein-7 group has a weaker tendency of EndMT and fibrosis.Conclusions TGF-β1 belongs to a main mediating factor with a tendency of heart fibrosis.It can guide EndMT and resist TGF-β1 and heart fibrosis.
