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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 investigate the effect of eNOS gene transfection with JAK1 / STAT3 on angiogenesis after myocardial infarction (MI). Methods Wistar rats were used to establish gene transfection and myocardial infarction models. The effects of eNOS gene transfection on the protein expression of signaling pathway, cardiac function and angiogenesis were observed. Results Compared with the control group, the eNOS expression was significantly increased, the expression of JAK1 / STAT3 was significantly increased, and NO production was significantly increased after eNOS gene transfection ([0.42 ± 0.04] nmol / mg vs (0.18 ± 0.02) nmol / mg] 0.01). The area of MI decreased and the formation of blood vessels increased obviously. The function of heart improved obviously on the 7th day after MI. Conclusions The area of MI after eNOS gene transfection is significantly reduced, cardiac function is improved obviously, angiogenesis is obviously increased. The effect of eNOS gene on the angiogenesis after MI may be related to the increase of JAK1 / STAT3 expression.