【摘要】 目的研究蜈蚣酸性蛋白(CAP)对血管紧张素-Ⅱ(AngⅡ)诱导培养心肌细胞凋亡的影响及机制。方法在培养原代乳鼠心肌细胞的基础上,通过MTT法观察CAP对培养心肌细胞活力的影响;采用激光共聚焦显微镜观察细胞凋亡情况;使用半胱胺酸-天门冬胺酸酶(caspase-3)活性检测试剂盒,分光光度法检测心肌细胞凋亡过程中caspase-3活性的变化;并采用半定量逆转录聚合酶链反应(RT-PCR)法测定相关基因c-fos mRNA表达。结果 AngⅡ模型组与空白对照组比较,心肌细胞活力明显降低,凋亡明显增加;Caspase-3活性显著增加;c-fos mRNA的表达显著增加。CAP高、低剂量组与AngⅡ模型组比较,心肌细胞活力明显增加,凋亡明显降低;Caspase-3活性显著降低,c-fos mRNA的表达显著降低。结论 CAP对AngⅡ诱导的心肌细胞凋亡具有明显的抑制作用,其机制与降低Caspase-3活性以及下调c-fos mRNA表达有关。更多还原

【Abstract】 Objective To study the influence of centipede acidic protein ( CAP) on myocardial apoptosis induced by angiotensin II ( AngII ) and the mechanism. Methods On the base of culturing cardiomyocytes in neonatal rats,the influence of CAP on cardiomyocyte viability was observed by using MTT method. The apoptosis was observed by using laser scanning confocal fluorescence microscope. The changes of caspase-3 activity during cardiomyocyte apoptosis were detected by using spectrophotometry with Caspase-3 Activity Assay Kit. The expression of c-fos-mRNA was detected by using RT-PCR. Results The cardiomyocyte viability decreased significantly,and cardiomyocyte apoptosis,caspase-3 activity and expression of c-fos-mRNA increased significantly in the AngII model group compared with the blank control group. The cardiomyocyte viability increased significantly,and cardiomyocyte apoptosis, caspase-3 activity and expression of c-fos-mRNA decreased significantly in the high-dose and mid-dose CAP groups compared with the AngII model group. Conclusion CAP inhibits significantly the cardiomyocyte apoptosis induced by AngII,and the mechanism is related to the decreases of caspase-3 activity and expression of c-fos-mRNA.更多还原