摘要
目的探讨JAK1/STAT3参与的eNOS基因转染对心肌梗死(MI)后血管形成的影响。方法采用Wistar大鼠,建立基因转染和心肌梗死模型,观察eNOS基因转染对信号通道蛋白表达、心脏功能和血管形成的影响。结果与对照组比较,eNOS基因转染后,eNOS表达明显增加、JAK1/STAT3表达明显增加、NO生成明显提高[(0.42±0.04)nmol/mgvs.(0.18±0.02)nmol/mg](P<0.01)、MI面积减少、血管形成明显增加,MI后7d心脏功能明显改善。结论 eNOS基因转染后MI面积明显减少、心脏功能明显改善,血管形成明显增加;eNOS基因对MI后血管形成的作用可能与增加JAK1/STAT3的表达有关。
Objective To study the effects of JAK/STAT3-involved endothelial nitric oxide synthase(eNOS) gene transfer on the angiogenesis after myocardial infarction(MI).Methods Human eNOS gene in an adenovirus vector was delivered locally into male Wistar rats heart 4 days prior to MI induced by left anterior descending coronary artery ligation.Neovascularization was identified immunohistochemically.Expression of JAK1/STAT3 was detected by Western blot.ResultsCompared to the controls,eNOS gene transfer significantly increased the expressions of eNOS and JAK1/STAT3 and production of NO,stimulated the angiogenesis,reduced myocardial infarct size and improved cardiac contractility on the 7th day after MI.Conclusion eNOS/NO system provides cardiac protection on MI injury through stimulates angiogenesis and action of JAK1/STAT3 signaling.
出处
《江苏医药》
CAS
CSCD
北大核心
2010年第19期2303-2305,F0003,共4页
Jiangsu Medical Journal
关键词
心肌梗死
ENOS基因
JAK1/STAT3
Myocardial infarction
Endothelial nitric oxide synthase gene (eNOS gene)
JAK1/STAT3