CAJ | 학술논문

目的：本研究探讨β2糖蛋白Ⅰ（β2GPⅠ）能否协同脂多糖（LPS）激活肝癌细胞SMMC-7721核因子（NF-κB）的活化及下游因子（TNF-α、IL-1β、AFP）的表达。方法实验分为四大组：A组：空白细胞（SMMC-7721）组，B组：β2GPⅠ转染组，C组：低、中、高浓度（1、10、100 ng/ml）LPS作用组， D 组：β2GPⅠ联合低、中、高浓度（1、10、100 ng/ml）LPS 作用组。通过激光共聚焦分析法分析 NF-κB的活化情况，酶联免疫吸附法分析下游因子（TNF-α、IL-1β、AFP）的表达情况。结果 B、C、D 三组的NF-κB均有不同程度活化。D组β2GPⅠ联合LPS组活化最明显，并且下游因子TNF-α、IL-1β、AFP表达较其他组显著增加，差异有统计学意义（P＜0.05），且呈浓度依赖性。结论 LPS能增强β2GPⅠ对肝癌细胞内的信号传导，激活 NF-κB，启动下游信号转导，增加下游因子的表达，可能在促进肝癌的发生发展过程中起到一定的作用。
목적：본연구탐토β2당단백Ⅰ（β2GPⅠ）능부협동지다당（LPS）격활간암세포SMMC-7721핵인자（NF-κB）적활화급하유인자（TNF-α、IL-1β、AFP）적표체。방법실험분위사대조：A조：공백세포（SMMC-7721）조，B조：β2GPⅠ전염조，C조：저、중、고농도（1、10、100 ng/ml）LPS작용조， D 조：β2GPⅠ연합저、중、고농도（1、10、100 ng/ml）LPS 작용조。통과격광공취초분석법분석 NF-κB적활화정황，매련면역흡부법분석하유인자（TNF-α、IL-1β、AFP）적표체정황。결과 B、C、D 삼조적NF-κB균유불동정도활화。D조β2GPⅠ연합LPS조활화최명현，병차하유인자TNF-α、IL-1β、AFP표체교기타조현저증가，차이유통계학의의（P＜0.05），차정농도의뢰성。결론 LPS능증강β2GPⅠ대간암세포내적신호전도，격활 NF-κB，계동하유신호전도，증가하유인자적표체，가능재촉진간암적발생발전과정중기도일정적작용。
Objective The objective of this study was to elucidate whether beta2-GPⅠ interacts with LPS to increase the activation of NF-κB and the expression of TNF-α, IL-1β and AFP in liver cancer cell SMMC-7721. Methods NF-κB activation was assessed by immunofluorescence assay in SMMC-7721 HCC cells exposed to various treatments. The cells were normal control cells (group A), transiently transfected with vectors expressing beta2-GPⅠ(group B), incubated with different concentrations (1,10,100 ng/ml) LPS (group C1-C3) and group D1-D3 were incubated with different concentrations (1,10,100 ng/ml) LPS and transfected with beta2-GPⅠvector. TNF-α, IL-1β, AFP expression were detected by ELISA in all groups. Results Group B, C and D had induced activation of NF-κB. However, the highest activity of NF-kB was observed in group D3. The mean TNF-α, IL-1β and AFP levels were significantly higher in group D3 than other groups with significant differences (P<0.05) on concentration-dependent manner. Conclusion Beta2-GPⅠ can interact with LPS and then play a role in the development of HCC by activating NF-κB.