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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 whether MAPK signal transduction pathway is involved in the pathogenesis of portal hypertension. Methods Experimental group of hepatitis B cirrhosis in patients with portal hypertension in 18 cases, hospitalized during selective elective splenectomy plus cardia around the vascular surgery. In the control group, 10 cases of splenectomy patients admitted to hospital due to traumatic splenic rupture during the same period were selected. Western blot was used to detect the expression of phosphorylated extracellular signal-regulated kinase (ERK1 / 2) in total spleen tissue. The expression of cfos in splenic vein tissue was observed by immunohistochemistry. Results The activity of ERK1 / 2 in the splenic vein of experimental group was significantly higher than that of normal group (P <0.01). The expression of cfos in the splenic vein wall was increased in the experimental group, with an average staining index of 6.2675 ± 0.3124. The cfos expression in the splenic vein wall was increased in the normal group with an average staining index of 1.8213 ± 0.5041 (P <0.01). cfos is strongly positive in smooth muscle cells. Conclusion The ERK1 / 2 / cfos signaling pathway is associated with the development of portal hypertension. ERK1 / 2 / cfos signaling pathway may be an important regulatory pathway of vascular smooth muscle cell phenotype.