摘要
目的探讨丝裂原激活蛋白激酶(MAPK)信号传导通路是否参与门静脉高压性血管病变的发生过程。方法实验组为乙肝后肝硬化门静脉高压症患者18例,住院期间行择期脾切除加贲门周围血管离断术。对照组选取同期因外伤性脾破裂急诊入院行脾切除术患者10例。采用Westernblot方法检测脾静脉组织总蛋白中磷酸化细胞外信号调节激酶丝裂原ERK1/2的表达。采用免疫组织化学方法观察cfos在脾静脉组织中的表达情况。结果实验组脾静脉壁ERK1/2活性较正常组明显增高(P<0.01)。实验组脾静脉壁cfos表达增高,平均染色指数为6.2675±0.3124,正常组脾静脉壁cfos表达增高,平均染色指数为1.8213±0.5041,两者比较差异有统计学意义(P<0.01)。cfos在平滑肌细胞中强阳性表达。结论ERK1/2/cfos信号传导途径与门静脉高压性血管病变的发生有关,ERK1/2/cfos信号传导途径可能是血管平滑肌细胞表型转变的重要调控途径。
Objective To investigate the roles of mitogen-activated protein kinase （MAPK） signal transduction pathway in the pathogenesis of portal hypertensive vasculopathy. Methods Eighteen patients with posthepatitic cirrhosis portal hypertension （ 12 males and 6 females） admitted to Tongji Hospital were subjected to splenectomy plus pericardial devascularization during hospitalization served as experimental group, while 10 patients （7 males and 3 females） with traumatic spleen rupture subject to splenectomy during the same period as the control group. Phosphated ERK1/2 in total protein of spleen vein vessel from portal hypertensive patients was detected by Western blot, and c-fos expression in splenic vein vessel by immunohistochemical method. Results The expression of phosphated ERK1/2 in splenic vein of the patients with portal hypertension was higher than in control group （ P〈0.01 ）, The expression of c-fos in the splenic vein in experimental group and control group was increased with the average staining index being 6.267 5±0.312 4 and 3.050 0±0.300 5 respectively. The strong expression of c-fos was detected in vascular smooth muscle ceils. Conclusion ERK1/2/c-fos signal transduction pathway may play an important role in the pathogenesis of portal hypertensive vasculopathy, MAPK may participate in the process of phenotype modulation of vascular smooth muscle cells.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2005年第9期1066-1067,共2页
Chinese Journal of Experimental Surgery
基金
国家自然科学基金资助项目(30170920)
