高速枪弹压力波调控内皮细胞ET-1的信号通路  

TX Primary study on signaling pathway in transduction of pressure wave created by high velocity projectiles to modulating ET-1 in cultured endothelial cells

作　　者：赖西南 官正华[1] 李曙光[1] 张良潮[1] 安波[1] 王建民[1] 王大田[1] 吴国萍[1] 陈蕾[1] 

机构地区：[1]第三军医大学大坪医院野战外科研究所

出　　处：《中国病理生理杂志》1998年第1期75-78,共4页Chinese Journal of Pathophysiology

摘　　要：目的和方法：以高速枪弹压力波致伤培养细胞为实验模型，以特异的Ｇ蛋白和肌醇磷脂代谢抑制剂作用培养内皮细胞，力图从分子创伤学角度探讨压力波调控ＥＴ－１的信号通路。结果：磷脂酶Ｃ抑制剂ｎｅｏｍｙｃｉｎ作用内皮细胞，明显消除压力波对ＥＴ－１释放及表达的刺激作用。Ｇ蛋白抑制剂ＧＤＰ－β－Ｓ则无明显作用。蛋白激酶Ｃ抑制剂ｓｌａｕｒｏｓｐｏｒｉｎｅ对压力波作用后ＥＴ－１基因表达增强有较强的抑制作用。结论：高速枪弹压力波对内皮细胞ＥＴ－１的调控可能通过某种直接途径（而非Ｇ蛋白介导）激活肌醇磷脂代谢，从而生成ＩＰ３和二酰基甘油。ＩＰ３可能参与早期ＥＴ－１释放，二酰基甘油对ＰＫＣ的激活参与了ＥＴ－１基因表达的调控。AIM:To explore adding special signaling inhibitores to the cultured endothelial cells which was affected by the pressure wave METHODS:The cultured human umbilical vein endothlial cells were exposed to the short lasting burst pressure wave caused by 7 62mm military bullet penet rating water, the positive peak implitude was 170kPa, and specific inhibitors to phospholipase C, protein kinase C and G protein were added separately to culture media lh before pressure wave effecting the cells RESULTS: Neomycin, specific inhibitor to phospholipase C , abolished the increase of ET-1 release and gene expression, whereas GDP-β-,G-protein inhibitor, was not effective As adding staurosporine, protein kinase C inhibitor, gene expression was depressed only CONCLUSION: Pressure wave regulating ET-1 secretion and mRNA might be result from activating phosphoinositide turnover directly and not through G protein

关 键 词：创伤 枪弹伤 压力波 内皮细胞 ET-1 

分 类 号：R826.502[医药卫生—临床医学]