CAJ | 학술논문

目的：观察金黄色葡萄球菌感染人巨噬细胞系U937细胞后信号通路Toll样受体4(TLR4)-p38蛋白激酶(p38MAPK)的表达及意义。方法体外培养人巨噬细胞系U937细胞,感染0、30、60和90 min 时收集细胞,应用Western blot法检测各组TLR4和p38MAPK蛋白表达的变化；在另一实验中,分为对照组、金黄色葡萄球菌感染60 min组及p38MAPK 抑制剂SB2035805 mg/mL干预组、SB20358010 mg/mL干预组,应用Western blot法检测各组TLR4和p38MAPK蛋白表达的变化。结果随着感染时间的延长,TLR4和p38MAPK蛋白的表达逐渐增加；给予SB203580抑制剂后,TLR4和p38MAPK蛋白的表达明显减弱。结论金黄色葡萄球菌感染U937细胞可引起TLR4-p38MAPK信号通路的活化,而SB203580对其有明显的抑制作用,证明TLR4-p38MAPK信号通路与金黄色葡萄球菌感染U937细胞密切相关。
목적：관찰금황색포도구균감염인거서세포계U937세포후신호통로Toll양수체4(TLR4)-p38단백격매(p38MAPK)적표체급의의。방법체외배양인거서세포계U937세포,감염0、30、60화90 min 시수집세포,응용Western blot법검측각조TLR4화p38MAPK단백표체적변화；재령일실험중,분위대조조、금황색포도구균감염60 min조급p38MAPK 억제제SB2035805 mg/mL간예조、SB20358010 mg/mL간예조,응용Western blot법검측각조TLR4화p38MAPK단백표체적변화。결과수착감염시간적연장,TLR4화p38MAPK단백적표체축점증가；급여SB203580억제제후,TLR4화p38MAPK단백적표체명현감약。결론금황색포도구균감염U937세포가인기TLR4-p38MAPK신호통로적활화,이SB203580대기유명현적억제작용,증명TLR4-p38MAPK신호통로여금황색포도구균감염U937세포밀절상관。
Objective To investigate the effect and significance of TLR4 and p38MAPK signaling pathway expressed in human monocytic U937 cells infected by Staphylococcus aureus. Methods U937 cells were infected by Staphylococcus aureus were collected at 0,30,60 and 90 min after infection respectively,and Western blot was per-formed to detect the expressions of TLR4 and p38MAPK. In another experiment,the routinely cultured U937 cells in vitro were divided into control group,Staphylococcus aureus stimulation group,SB203580(5 mg/mL or 10 mg/mL) plus Staphylococcus aureus treatment groups. Western blot was performed to detect the expressions of TLR4 and p38MAPK. Results The expressions of TLR4 and p38MAPK increased in a time-dependent manner. Compared with those in the control group,the expressions of TLR4 and p38MAPK increased more significantly in U937 cells induced by Staphylococcus aureus. SB203580 could effectively inhibit the expressions of TLR4 and p38MAPK. Conclusion The TLR4-p38MAPK signaling pathway can be activated by Staphylococcus aureus in U937 cells,and SB203580 sig-nificantly inhibits the signaling pathway,demonstrating the close relation between the TLR4-p38MAPK signaling path-way in Staphylococcus aureus-infected U937 cells.