摘要
目的通过对比研究磷酸化信号转导与转录激活因子(P-STAT3)、乙烯基鳞片胶泥(VEGF)和碱性成纤维细胞生长因子(BFGF)在门静脉高压症(PHT)患者脾脏组织中的表达,探讨JAK2/STAT3通路在PHT内脏高动力循环形成过程中的机制。方法收集收治的乙肝肝硬化PHT患者60例(病例组)、外伤性脾破裂患者20例(对照组),采用免疫组织化学方法对比研究2组患者脾脏组织中P-STAT3、VEGF和BFGF的表达情况。结果病例组中P-STAT3、VEGF及BFGF的表达灰度值分别为146.21±11.34、136.65±14.52和156.54±19.82,对照组中分别为45.18±8.25、37.36±7.43和48.65±10.15,病例组明显高于对照组(P<0.05)。病例组脾脏组织中P-STAT3、VEGF和BFGF在术前肝功能Child-Pugh分级(A级、B级)和上消化道出血病史(有、无)的组间表达差异无统计学意义(P>0.05);而在脾脏肿大程度(轻、中、重度)和脾功能亢进程度(轻、中、重度)的组间表达差异有统计学意义(P<0.05)。P-STAT3和BFGF在静脉曲张程度(轻、中、重度)组间表达差异无统计学意义(P>0.05);但VEGF在静脉曲张程度(轻、中、重度)组间表达差异有统计学意义(P<0.05)。结论 JAK2/STAT3信号通路的激活能促进PHT患者内脏高动力循环状态形成,并参与患者脾肿大、脾功能亢进及食管胃底静脉曲张等病理生理过程。
Objective To study the mechanism of JAK2/STAT3 pathway in the formation of visceral hyperdynamic circulation in patients with portal hypertension through investigating the expression of P - STATS, VEGF and BFGF in the patient＇ s spleen. Methods Data of sixty patients with portal hypertension after hepatitis B infection （ the experimental group） and twenty patients with spleen rupture after trauma（the control group） were accumulated. The immunohistochemistry technique was used to investigated the ex- pression of P - STAT3 ,VEGF and BFGF in the spleen tissues in two groups. Results The expression of P - STAT3 ,VEGF and BFGF were 146.21 ± 11. 34,136.65 ± 14.52,156.54 ± 19.82 in experimental group and 45.18 ±8.25,37.36 ±7.43,48.65 ± 10.15 in the control group,respectively. It were significantly higher in the experimental group compared with the control group （ P 〈 0.05 ）. In patients with portal hypertension,the expression of P -STATS,VEGF and BFGF were not different among the different preoperative liver functional groups （Child- Pugh A or B） and groups with or without intestinal haemorrhage history,but it was significantly different- between the different groups of mild, moderate or severe splenomegaly and mild moderate or severe hypersplenism （ P 〈 0.05）. The expression of VEGF was different between different varices groups（ mild moderate or severe） while the expression of P - STATS and BFGF were not different in these groups. Conclusion The activation of JAK2/STATS pathway induced the formation of visceral hyperdynamic circulation in patients with portal hypertension and participated the pathophysiological procedure of splenomegaly hypersplenism and varices.
作者
杨勇
刘明奇
田明国
贾东
辛国军
丁洋
YANG Yong;LIU Mingqi;TIAN Mingguo;JIA Dong;XIN Guojun;DING Yang(Ningxia people＇s Hospital, Yinchuan 750002, Chin)
出处
《宁夏医学杂志》
CAS
2018年第4期292-295,共4页
Ningxia Medical Journal
基金
宁夏自然科学基金资助项目(NZ14294)
