核因子-κB及其调控产物在实验性自身免疫性肝炎中的表达及意义  

Expression of NF-κB and its regulation products in experimental autoimmune hepatitis and its significance

作　　者：杨兰兰[1] 鲍启德[2] 崔东来[3] 王彦[1] 

机构地区：[1]河北大学护理学院,河北省保定市071000 [2]河南安阳地区医院消化内科,河南省安阳市455000 [3]河北医科大学第二医院消化内科,河北省石家庄市050000

出　　处：《世界华人消化杂志》2008年第8期892-895,共4页World Chinese Journal of Digestology

摘　　要：目的:观察实验性自身免疫性肝炎(experi- mental autoimmune hepatitis,EAH)肝组织中核因子-κB(nuclear factor kappa B,NF-κB)及其调控产物细胞间黏附分子-1(intercellular adhesion molecule-1,ICAM-1)、肿瘤坏死因子-α(tumor necrosis factorα,TNF-α)和白细胞介素-6(interleukin-6,IL-6)在EAH中的表达和在肝损伤中的作用.方法:采用肝抗原S-100与弗氏完全佐剂充分乳化后,予d1、7、14和21 C57BL/6小鼠ip诱导EAH模型,于d 28处死所有小鼠.免疫组织化学方法观察NF-κB、ICAM-1、TNF-α、IL-6的表达.结果:对照组肝细胞以中央静脉为中心向四周呈放射状排列,汇管区无炎症浸润,EAH模型组小鼠肝组织学可见肝细胞片状坏死和淋巴细胞浸润.对照组中未观察到NF-κB、ICAM-1、TNF-α和IL-6的表达,而模型组中均有阳性表达.结论:NF-κB通过调控ICAM-1、TNF-α和IL-6的基因表达,NF-κB及其调控产物可能在EAH的肝细胞损伤过程中起着重要的作用.AIM： To investigate the factor kappa B （NF-κB）, expression of nuclear intercellular adhesion molecule-1 （ICAM-1）, tumor necrosis factor-α （TNF-α） and interleukin-6 （IL-6） in experimental autoimmune hepatitis （EAH） model and to explore the role of those molecules in liver injury of EAH. METHODS： EAH model was induced by intraperitoneal injection of syngeneic S-100 antigen emulsified in complete Freud＇s adjuvant into C57BL/6 on days 1, 7, 14 and 21. On the 28 day, animals were killed. Expressions of NF-κB, ICAM-1, TNF-α and IL-6 were observed using histoimmunochemistry. RESULTS： Liver cells in the control group wereradially arranged from the central venous to the all sides. No inflammatory infiltration was observed in the portal area. Histology showed patchy necrosis of liver cells and lymphocyte infiltration in the EAH model. NF-κB, ICAM-1, TNF-α and IL-6 were not expressed in the control group but positively expressed in the model group. CONCLUSION： NF-κB and its regulation products play an important role in the process of hepatic cell injury by regulating the expression of ICAM-1, TNF-α and IL-6.

关 键 词：实验性自身免疫性肝炎 核因子-ΚB 小鼠 

分 类 号：R575.1[医药卫生—消化系统]