脾脏核转录因子κB表达对肝缺血再灌注损伤的影响  

The nuclear transcription factor-κB expression in spleen influence on acute hepatic cell injury induced by liver warm ischemia reperfusion in rats

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作  者:孟凡强[1] 宁武[1] 裴东坡[1] 张东东[1] 李超丰[1] 周雷[1] 王文跃[1] 姜洪池[2] 

机构地区:[1]中日友好医院普外科,北京100029 [2]哈尔滨医科大学第一临床医学院普外科,哈尔滨150001

出  处:《中日友好医院学报》2011年第3期164-166,170,F0002,共5页Journal of China-Japan Friendship Hospital

摘  要:目的:探讨脾脏在大鼠肝缺血再灌注(HIR)损伤中的作用及其机制。方法:采用阻断和恢复大鼠全肝血供,肝缺血30min再灌注180min。雄性Wistar大鼠随机分为假手术组(SHAM组)、脾切除加再灌注组(SPLN+HIR组)和再灌注组(HIR组)。血清谷草转氨酶(AST)、谷丙转氨酶(ALT)水平检测肝功状况,苏木素-伊红(HE)染色观察肝脏及脾脏病理形态学改变,流式细胞仪检测肝细胞凋亡率,干湿比(W/D)比较肝脏水肿程度,髓过氧化物酶(MPO)水平测定肝脏中性粒细胞浸润情况,ELISA法测定血清TNF-α水平,SP法检测脾脏核转录因子(NF)-κB表达情况。结果:HIR组肝脏受到严重损伤,表现为AST、ALT、W/D显著升高,病理形态学改变明显,凋亡细胞大量出现,大量中性粒细胞浸润。SPLN+HIR组上述病理改变较轻,血清TNF-α平较低。HIR组脾脏病理形态改变明显,脾脏NF-κB高表达。结论:脾脏对HIR损伤起重要的促进作用,可能是HIR期间脾细胞中NF-κB被大量激活,引起TNF-α水平升高,进而加重或激发肝细胞凋亡。Objective:To investigate the reason that splenectomy could ameliorate hapatic damage caused by hepatic I/R(ischemia/reperfusion).Methods:Wistar rats randomly assigned into three groups underwent sham-operation,hepatic ischemia reperfusion induced by total hepatic vascular occlusion,and splenectomy plus hepatic ischemia reperfusion,respectively.Blood samples were collected for assessing serum levels of AST,ALT and TNF-α,while activities of Myeloperoxidase(MPO)in liver were examined.Livers underwent histopathologic examination for injury severity,and FCM for cell apoptosis.Expressions of nuclear transcription factor-κB(NF-κB)in spleen tissues were detected with SP method.Results:Hepatic I/R resulted in liver injury,evidenced by morphologic alteration,elevated W/D and serum levels of AST and ALT,and increased apoptotic cells.The activity of MPO in liver tissues and the serum level of TNF-α were increased after I/R.However,splenectomy significantly protected the liver from I/R injury just as our previous study.The expression of NF-κB was up regulated in spleen tissues by hepatic I/R.Conclusion:Prior splenectomy protects liver from injury by hepatic I/R.This study has demonstrated that NF-κB in spleen has been activated,then release of TNF-α.The mechanism needs further investigation.

关 键 词: 再灌注损伤 凋亡 大鼠 

分 类 号:R363[医药卫生—病理学]

 

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