CAJ | 학술논문

目的探讨利多卡因对LPS诱导大鼠腹腔巨噬细胞NF-κB活性的影响.方法取wistar大鼠腹腔巨噬细胞,以2 × 106/ml的密度接种于12孔培养板,每孔1 ml.纯化处理后随机分为5组,每组10孔.正常对照组(C组)加入RPMI-1640培养液1 ml,L组加入含100 ng/ml LPS的RPMI1640培养液1 ml,LL1组、LL2组和LL3组分别加入含有2、20、200μg/ml利多卡因+100 ng/ml LPS的RPMI-1640培养液1 ml.孵育24 h后,收集上清液,测定高迁移率族蛋白B1(HMGB1)浓度;取细胞沉淀,测定HMGBl mRNA表达水平和NF-κB活性.结果与C组比较,其他各组HMGB1浓度、HMGB1mRNA表达和NF-κB活性均升高(P＜0.05);与L组及LL1组比较,LL2组和LL3组上述指标降低(P＜0.05).LL3组HMGB1 mRNA表达水平低于LL2组(P＜0.05).结论利多卡因可抑制LPS诱导大鼠腹腔巨噬细胞NF-κB活化,从而抑制HMGB1的合成与释放.
목적 탐토리다잡인대LPS유도대서복강거서세포NF-κB활성적영향.방법 취wistar대서복강거서세포,이2 × 106/ml적밀도접충우12공배양판,매공1 ml.순화처리후수궤분위5조,매조10공.정상대조조(C조)가입RPMI-1640배양액1 ml,L조가입함100 ng/ml LPS적RPMI1640배양액1 ml,LL1조、LL2조화LL3조분별가입함유2、20、200μg/ml리다잡인+100 ng/ml LPS적RPMI-1640배양액1 ml.부육24 h후,수집상청액,측정고천이솔족단백B1(HMGB1)농도;취세포침정,측정HMGBl mRNA표체수평화NF-κB활성.결과 여C조비교,기타각조HMGB1농도、HMGB1mRNA표체화NF-κB활성균승고(P＜0.05);여L조급LL1조비교,LL2조화LL3조상술지표강저(P＜0.05).LL3조HMGB1 mRNA표체수평저우LL2조(P＜0.05).결론 리다잡인가억제LPS유도대서복강거서세포NF-κB활화,종이억제HMGB1적합성여석방.
Objective To investigate the effect of lidocaine on the LPS-induced NF-κB activity in rat peritoneal macrophages. Methods The peritoneal macrophages obtained from male Wistar rats were placed in 12-well plates at 2 × 106 cell/ml after being cultured for 3 days. Each well contained 1 ml of cell suspension. The cells were randomized into control group (group C), LPS group and 3 LPS + lidocaine group S (group LL1.2.3)(n = 10 wells each). In group LPS and LL1,2,3, the cells were exposed to LPS 100 ng/ml. In group LL1,2,3 the cells were exposed to lidocaine 2, 20 200 kg/ml respectively in addition to LPS 100 ng/ml. After being incubated for 24 h, the HMGB1 concentration in the supernatant (by ElISA) and HMGB1 mRNA expression (by RT-PCR)and NF-κB activity in the cells were measured. Results LPS signiticantly increased HMGB1 concentration,HMGB1 mRNA expression and NF-κB activity in the supernatant. Lidocaine treatment significantly attenuated the LPS-induced increase in HMGB1 concentration HMGB1 mRNA expression and NF-κB activity in a dose-dependent manner. Conclusion Lidocaine can inhibit NF-κB activity in the rat peritoneal macrophages and in turn inhibit the synthesis and release of HMGB1.