SN50对缺血再灌注损伤中TNF-α影响的实验研究  

Experimental study of SN50 on TNF-α effects in ischemia-reperfusion injury

作　　者：吴勇[1] 叶芬[1] 葛轶睿[1] 陆燕[1] 魏锐利[2] 

机构地区：[1]第二军医大学南京临床医学院(南京军区南京总医院)眼科,江苏南京210002 [2]第二军医大学附属长征医院眼科,上海200003

出　　处：《东南国防医药》2014年第5期453-455,共3页Military Medical Journal of Southeast China

基　　金：国家自然科学基金(81200719)

摘　　要：目的研究核转录因子-κB(nuclear factor-kappaB,NF-κB)抑制剂SN50对氧糖剥夺条件下培养的SD大鼠巨噬细胞炎性因子肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)表达的影响。方法用MTT法检测SN50对细胞增殖活性的影响,以ELISA法检测氧糖剥夺条件下SN50对TNF-α表达影响。结果经SN50处理的氧糖剥夺条件下的巨噬细胞成活率较未经处理的明显上升(P<0.05或P<0.01),TNF-α表达的上调幅度亦明显变小(P<0.05或P<0.01)。结论 SN50主要是通过抑制NF-κB核的移位干扰了TNF-α的基因转录而导致其合成的蛋白量降低。Objective To study the effect of SN50,the nuclear factor kappa B（ NF-κB） inhibitor on the expression of macrophage inflammatory factor TNF-α in the oxygen and glucose deprivation in SD rats. Methods The effect of SN50 on cell proliferation activity was observed by MTT method. The expression of TNF-α in macrophages after treated with SN50 was observed by ELISA. Results The macrophage survival rate was significantly increased after treated with SN50（ P〈0. 05 or P〈0. 01）. The increase of TNF-α was significantly smaller after treated with SN50 in oxygen glucose deprivation conditions（ P〈0. 05 or P〈0. 01）. Conclusion SN50 reduces the expression of TNF-α in macrophages,mainly through inhibiting the translocation of NF-κB nuclear,which provides a theoretical basis for the clinical treatment of ischemic reperfusion injury.

关 键 词：SN50 巨噬细胞 肿瘤坏死因子-Α 核转录因子-ΚB 缺血再灌注 

分 类 号：R363[医药卫生—病理学]