论文部分内容阅读
目的 本文旨在研究腺病毒介导的成年小鼠心肌直接PKCε基因转移对左室收缩功能的影响。方法 使用标准方法建立表达PKCε基因的重组腺病毒载体。直接注射重组腺病毒到FVB/N和ICR小鼠心肌 ,对照鼠给予相同剂量空载腺病毒。Western免疫印迹测定PKCε蛋白质表达水平。用非开胸经颈总动脉插管的显微外科技术评价小鼠左室收缩功能。结果 与对照鼠相比基因转移鼠心肌转基因PKCε蛋白质表达水平增加近 4倍 ,基线左室最大收缩压、最大收缩速率 (dP/dt)、 -dP/dt明显降低 ,左室舒张末压、舒张压明显升高 (p <0 0 1) ,异丙肾上腺素激发后左室dP/dt剂量依赖的升高明显减弱 (p <0 0 1) ,PKCε基因转移鼠心脏 /体重比也较对照鼠明显增加 (p <0 0 1)。结论 腺病毒介导的、心肌直接的PKCε基因转移诱发了左室收缩功能的损害 ,导致了心肌肥厚和心衰。
Objective This study aimed to investigate the effect of adenovirus mediated direct myocardial PKCε gene transfer on left ventricular systolic function in adult mice. Methods The recombinant adenovirus vector expressing the PKCε gene was established using standard methods. Direct injection of recombinant adenovirus into FVB / N and ICR mouse myocardium, control mice were given the same dose of empty vector. Western blot was used to determine PKCε protein expression. Evaluation of left ventricular systolic function using non-thoracotomy with common carotid artery by microsurgical techniques. Results Compared with control mice, the expression of PKCε protein in gene transfer myocardium increased nearly fourfold, and the maximal systolic and maximal rates of left ventricular systolic pressure (dP / dt) and -dP / dt were significantly decreased in baseline LV diastolic and diastolic (P <0.01), the dose-dependent increase of dP / dt in left ventricular after isoproterenol challenge was significantly attenuated (p <0.01), and the cardiac / body weight ratio of PKCε gene-transferred mice was also significantly higher than that of control rats Significantly increased (p <0.01). Conclusions Adenovirus-mediated, direct myocardial PKCε gene transfer induces impairment of left ventricular systolic function leading to cardiac hypertrophy and heart failure.