心肌肥厚大鼠心肌组织中肌醇磷脂途径活性研究

Activation of phosphoinositide pathway in left ventricular tissue of rats with pressure overload induced cardiac hy- pertrophy

目的 观察肌醇磷脂信号传导通路在心肌肥厚形成中的作用。方法对大鼠行腹主动脉部分缩窄术制作心肌肥厚模型,术后10d处死动物测全心重/体重比值,以免疫印迹法测左心室组织Gαq/11蛋白含量,以放射免疫法测左心室组织1,4,5-三磷酸肌醇(IP3)含量,以非同位素法测蛋白激酶C(PKC)相对活性。结果术后10d时腹主动脉部分缩窄(CA)组大鼠全心重/体重比值明显高于假手术(SO)组(P<0.01),二组大鼠左心室组织Gαq/11蛋白含量无显著差异(P>0.05),CA组左心室组织IP3浓度明显高于SO组(P<0.05)。和SO组比较CA组左心室组织胞膜PKC活性升高但胞浆PKC活性降低(P均<0.05)。结论 肌醇磷脂途径参与压力超负荷性心肌肥厚病理过程。

Objective To investigate the role of phosphoinositide pathway in the formation of pressure-overload cardiac hypertrophy. Methods Cardiac hypertrophy was induced in male Sprague-Dawley rats with coarctation of abdominal aorta (CA), whole heart weight/body weight ratio was tested after 10 days. Content of Gaq/11 protein in left ventricle was detected by immunoblot analysis, concentration of inositol 1,4,5-trisphosphate (IP3) was measured by radioimmunoassay system and relative activity of protein kinase C(PKOwas determined by non-radioactive method. Results At 10 days,whole heart weight/body weight ratio of CA rats was higher than that of sham-operated (SO) animals (P<0. 01), content of Gaq/11 protein was not modified in left ventricle between two groups(P>0. 05) ,the level of 1P3 was significantly increased in the left ventricle of CA rats after 10 days of stenosis (P<0. 05). Compared with values of sham-operated animals, PKC activity was significantly increased in par-ticulate fraction but was significantly decreased in cytosolic fraction of CA rats (Both .P<0. 05). Conclusion Phosphoinositide pathway may play a role in the formation of cardiac hypertrophy induced by pressure overload.