摘要
目的 :探讨肌醇磷脂途径在压力超负荷性心肌肥厚形成中的作用。方法 :对SD大鼠行腹主动脉部分缩窄术复制心肌肥厚模型 ,术后 1 0d、30d时处死动物测全心重 /体重比值 ,以免疫印迹法测左室组织Gαq/ 1 1蛋白含量 ,以放免法测左室组织 1 ,4,5 -三磷酸肌醇 (IP3)含量。结果 :术后 1 0d和 30d时腹主动脉部分缩窄 (CA)组全心重 /体重比值均高于假手术 (SO)组 (P <0 0 1 ) ,在术后 1 0d和 30d两个时点两组大鼠左室组织Gαq/ 1 1蛋白含量均无显著差异 (P >0 0 5)。术后 1 0d时CA组大鼠左室组织IP3含量明显高于SO组 (P <0 0 5) ,但术后 30d时两组IP3含量无显著差异 (P >0 0 5)。结论
AIM: 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, whole heart weight/body weight ratio was tested after 10 or 30 days of operation. Content of Gαq/11 protein in left ventricle was detected by immunoblot analysis and concentration of IP 3 was measured by radioimmunoassay. RESULTS: At 10 and 30 days, whole heart weight/body weight ratio of coarctation aorta (CA) group was higher than that of sham-operated (SO) rats ( P< 0.01). Protein Gαq/11 contents were not modified after 10 or 30 days of stenosis ( P> 0.05). At 10 days, the level of IP 3 significantly increased in left ventricle of CA rats compared with the control animals ( P< 0.05), but there was no difference in IP 3 level between CA and SO group after 30 days of operation. CONCLUSION: Phosphoinositide signaling pathway may play a role in the early stage of cardiac hypererophy induced by pressure overload.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2002年第8期900-902,共3页
Chinese Journal of Pathophysiology
基金
国家自然科学基金资助项目 (No .39670 31 4 )