CAJ | 학술논문

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。
목적：연구핵전록인자-κB（ nuclear factor-kappaB，NF-κB）억제제SN50대양당박탈조건하배양적SD대서거서세포염성인자종류배사인자-α（ tumor necrosis factor-α，TNF-α）표체적영향。방법용MTT법검측SN50대세포증식활성적영향，이ELISA법검측양당박탈조건하SN50대TNF-α표체영향。결과경SN50처리적양당박탈조건하적거서세포성활솔교미경처리적명현상승（P＜0．05혹P＜0．01），TNF-α표체적상조폭도역명현변소（P＜0．05혹P＜0．01）。결론 SN50주요시통과억제NF-κB 핵적이위간우료TNF-α적기인전록이도치기합성적단백량강저。
Objective To study the effect of SN50,the nuclear factor kappa B (NF-κB) inhibitor on the expression of macro-phage inflammatory factor TNF-αin 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-αin macrophages after treated with SN50 was observed by ELISA.Re-sults The macrophage survival rate was significantly increased after treated with SN50 (P<0.05 or P<0.01).The increase of TNF-αwas 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-αin macrophages,mainly through inhibiting the translocation of NF-κB nuclear,which provides a theoretical basis for the clinical treatment of ischemic reperfusion injury.