摘要
目的观察失血性休克后，整合素链接激酶（ILK）在蛋白激酶C（PKC）α、ε调节失血性休克大鼠血管钙敏感性中的作用。方法观察抑制ILK对PKCα、ε激动剂的增高休克2h的Wistar大鼠肠系膜上动脉（SMA）血管环钙敏感性的影响，以及血管平滑肌细胞（VSMC）中PKCα、ε激动剂对ILK蛋白表达、活性的影响。结果PKCα、ε激动剂可显著增高失血性休克后SMA钙敏感性，使Ca2＋的Emax由正常对照组的47．2％分别增至66．5％和66．3％（P〈0．01）；抑制ILK可显著降低PKCα和ε激动剂的作用，Ca2＋的Emax分别降低至正常对照组的50．1％和56．2％（P〈0．01）。缺氧VSMC中，ILK蛋白表达和活性降低，PKCα、ε激动剂可增高缺氧VSMC的ILK蛋白表达和活性。结论PKCα、ε通过改变ILK的蛋白表达和活性，调节失血性休克血管钙敏感性。
Objective To observe the role of integrin-linked kinase （ILK） in the regulatory effects of protein kinase C （PKC） α and ε calcium sensitivity during hemorrhagic shock in rats. Methods The superior mesenteric artery （SMA） from Wistar rats were adopted to observe the influence of inhibitor of ILK on the effects of PKCα and ε agonists on calcium sensitivity after shock, and hypoxic vascular smooth muscle ceils （VSMC） were used to measure the protein expression and activity of ILK after applying PKCα and ε agonists following hypoxia. Results （ 1 ） The calcium sensitivity of SMA was decreased 2 h after shock, increased significantly by the agonists of PKCα and ε Emax of Ca2. was increased from 47. 2% to 66.5% and 66. 3% （P 〈0.01 ） of normal control respectively. The increasing effects of PKCα and ε agonist were weakened by the inhibitor of ILK,and the Emax of Ca2＋ was decreased to 50.1% and 56. 2% of normal control respectively （P 〈 0.01 ）. （2） The protein expression and activity of ILK in VSMC were decreased 2 h after hypoxia, and increased by the agonists of PKCα 2 h following hypoxia. Conclusion PKCα and ε regulates the calcium sensitization through changing the protein expression and activity of ILK following hemorrhagic shock in rats.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2009年第3期284-285,共2页
Chinese Journal of Experimental Surgery
基金
基金项目：国家重大基础研究计划“973”项目（2005CB522601）
国家杰出青年科学基金资助项目（30625037）
