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作 者:陈协辉[1] 梁进杰[1] 刘新荪 许云 CHEN Xie- hui LIANG Jin-jie LIU Xin-sun XU Yun(Department of Cardiology, Sun Yat-sen Cardiovascular Hospital, Shenz- hen, Guangdong, 518020, China)
机构地区:[1]深圳市孙逸仙心血管医院心内科,广东深圳518020 [2]深圳市福田区第二人民医院
出 处:《心血管康复医学杂志》2017年第3期245-250,共6页Chinese Journal of Cardiovascular Rehabilitation Medicine
基 金:深圳市科创委资助课题(JCYJ20130402145506089)~~
摘 要:目的:探讨人参皂苷Rg1对急性心肌梗死(AMI)大鼠冠状动脉新生血管形成的影响及其作用机制。方法:120只Wistar大鼠随机均分为假手术组(仅开胸暴露心脏,未结扎冠脉),AMI组(结扎左冠脉制模后不做任何处理)和人参皂苷组(在AMI模型制作3h后注射人参皂苷Rg1)。建模后第24h、1周和5周分别检测梗死面积,血管内皮生长因子(VEGF)及其受体(Flk-1)的表达,以及Ⅷ因子表达。结果:5周后,与假手术组比较,人参皂苷组和AMI组心肌梗死面积、微血管新生数、血管内皮生长因子(VEGF)及其受体Flk-1水平均明显增加(P<0.05或<0.01);与AMI组比较,人参皂苷组心肌梗死面积[(51.31±9.67)%比(29.33±6.70)%]明显减小,微血管新生数[(18.31±5.07)个比(46.79±13.67)个]、VEGF表达[灰度值:(84.3±8.7)比(32.9±16.7)](灰度值的高低与表达量成反比)、Flk-1表达[(17.6±8.7)个比(59.9±16.2)个]明显增多(P<0.05或<0.01)。结论:对于大鼠AMI模型,人参皂苷Rgl治疗,可动员骨髓干细胞归巢于缺血心肌,并上调VEGF和其受体Flk-1的表达,促进微血管生成,缩小心肌梗死面积。Objective, To explore influence of ginsenoside Rgl on coronary artery angiogenesis in rats with acute myocardial infarction (AMI) and its mechanism. Methods: A total of 120 Wistar rats were randomly and equally divided into sham op- eration group (only received thoracotomy to expose heart without coronary ligation) ,AMI group (no treatment after model development With ligating left coronary artery) and ginsenoside group (received ginsenoside Rgl injection on 3h after AMI model development). Infarct area, expressions of vascular endothelial growth factor (VEGF) and its receptor (Flk-1), and VIII factor expression were respectively measured on 24h, one week and five weeks after model development. Results: Compared With sham operation group after five weeks, there were significant rise in myocardial infarction area, number of new blood capillaries and expression levels of VEGF and its receptor Flk-1 in ginsenoside group and AMI group, P〈0.05 or 〈0.01 ; compared with AMI group, there was significant reduction in myocardial infarction area [ (51.31 ± 9. 67) % vs. (29. 33 ± 6. 70) %], and significant rise in number of new blood capillaries [(18. 31 ± 5. 07) vs. (46. 79 ± 13. 67)], expres- sions of VEGF [greyscale value: (84. 3 ± 8. 7) vs. (32. 9 ± 16. 7), greyscale value was inversely proportional to expression] and Flk-1 [(17. 6 ±8. 7) vs. (59. 9 ± 16. 2)] in ginsenoside group, P〈0. 05 or 〈0. 01. Conclusion.. Application of ginsenoside Rgl in AMI rat model can mobilize marrow stem cells gather in ischemic myocardium, upregulate expressions of VEGF and its receptor Flk-1, effectively promote angiogenesis of blood capillaries, and reduce myocardial infarction area.
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