摘要
目的研究核因子-κB(nuclearfactorkappaB,NF-κB)活性抑制剂对CCl4诱导急性肝损伤小鼠肝组织中细胞间黏附分子-1(intercellularashesionmolecule-1,ICAM-1)表达及肝功能的影响。方法30只雄性昆明小鼠(28±2.2)g随机分为3组,即正常对照组、急性肝损伤模型组和NF-κB活性抑制剂组。正常对照组腹腔注射生理盐水0.1mL/10g,实验组腹腔注射0.1%CCl40.1mL/10g,NF-κB活性抑制剂组于腹腔注射0.1%CCl40.1mL/10g前15min腹腔注射脯氨酸二硫代氨基甲酸酯(prothiocarbamatesDTC,ProDTC150μg/10g)1次,其后1次/d,共5次。结果模型组ALT、AST及MDA较正常组显著升高(P<0.01),SOD降低明显(P<0.01)。在正常组中肝脏无NF-κB、ICAM-1表达,肝损伤模型组中NF-κB有较强表达,ICAM-1在肝细胞坏死区强表达。NF-κB抑制剂组ALT、AST及MDA较模型组显著降低,NF-κB、ICAM-1表达均较肝损伤组减弱,肝组织坏死程度较轻。结论NF-κB在CCl4诱导小鼠急性肝损伤中表达明显增强,NF-κB抑制剂可减少NF-κB及ICAM-1表达并减轻肝损伤程度。
ObjectiveTo investigate the protective effects of nuclear factor kappa B(NF-κB)inhibitor on CCl4 induced acute liver injury in mice and subsequent expression of intercellular ashesion molecule-1(ICAM-1). MethodsMale Kunming mice[n=30,(28± 2.2 )g]were randomly divided into three test groups: normal control group, acute liver injury group and NF-κB inhibitor treatment group.Mice in the three groups were injected introperitoneally with sterile saline ( 0.1 mL/10 g), CCl4 ( 0.1 % , 0.1 mL/10 g) and prothiocarbamates DTC(ProDTC,150 μg/10 g) respectively,15 minutes later, the ProDTC group were further injected introperitoneally with CCl4 ( 0.1 % , 0.1 mL/10 g). The rejection lasted for five days, one time per day. ResultsCompared with normal control group,the levels of ALT,AST and MDA in mice of CCl4 model group increased singnificantly.SOD reduced abviously(P< 0.01 ).No expression of NF-κB,ICAM-1 in liver of control group. Compared with acute liver injury group, ProDTC treatment group significantly decreased the contents of NF-κB and ICAM-1 in liver, the levels of serum ALT, AST and hepatic homogenate MDA reduced significantly, which SOD in hepatic homogenate increased significantly. ConclusionProDTC as a NF-κB inhibitor can suppress NF-κB activation and subsequent expression of ICAM-1, improve acute liver injury induced by CCl4 in mice.
出处
《河北医科大学学报》
CAS
2006年第2期92-94,i0004,共4页
Journal of Hebei Medical University
