广西医学
廣西醫學
엄서의학
GUANGXI MEDICAL JOURNAL
2014年
10期
1374-1376
,共3页
杜学柯%廖品琥%潘灵辉%黄冰%葛万运%陈肖东
杜學柯%廖品琥%潘靈輝%黃冰%葛萬運%陳肖東
두학가%료품호%반령휘%황빙%갈만운%진초동
肺损伤%盐酸戊乙奎醚%白细胞介素-1β%A549 细胞%细胞间黏附分子-1
肺損傷%鹽痠戊乙奎醚%白細胞介素-1β%A549 細胞%細胞間黏附分子-1
폐손상%염산무을규미%백세포개소-1β%A549 세포%세포간점부분자-1
Lung injury%Penehyclidine hydrochloride%Interleukin-1β%A549 cell%Intercellular adhesion molecule-1
目的：探讨盐酸戊乙奎醚（PHC）抑制白细胞介素-1β（IL-1β）诱导 A549细胞分泌细胞间黏附分子-1（ICAM-1）及其作用机制。方法体外培养 A549细胞株，分别用培养液（A 组）、PHC （B 组）、IL-1β（C 组）和 IL-1β＋PHC（D 组）处理，NF-κB DNA 结合活性试剂盒检测刺激后1 h NF-κB DNA 结合活性；反转录-聚合酶链反应检测刺激后4 h ICAM-1 mRNA 表达；酶联免疫吸附法检测刺激后24 h ICAM-1蛋白表达。结果IL-1β刺激后，C 组 NF-κB DNA 结合活性、ICAM-1 mRNA 和蛋白明显升高（P ＜0．01），D 组 NF-κB DNA 结合活性、ICAM-1 mRNA 和蛋白高于 A 组（P ＜0．05），但低于 C 组（P ＜0．05），PHC 预处理能抑制 IL-1β诱导的 NF-κB DNA结合活性、ICAM-1 mRNA 和蛋白表达升高。结论PHC 可抑制 IL-1β诱导 A549细胞分泌 ICAM-1，其机制可能通过抑制 NF-κB 激活。
目的：探討鹽痠戊乙奎醚（PHC）抑製白細胞介素-1β（IL-1β）誘導 A549細胞分泌細胞間黏附分子-1（ICAM-1）及其作用機製。方法體外培養 A549細胞株，分彆用培養液（A 組）、PHC （B 組）、IL-1β（C 組）和 IL-1β＋PHC（D 組）處理，NF-κB DNA 結閤活性試劑盒檢測刺激後1 h NF-κB DNA 結閤活性；反轉錄-聚閤酶鏈反應檢測刺激後4 h ICAM-1 mRNA 錶達；酶聯免疫吸附法檢測刺激後24 h ICAM-1蛋白錶達。結果IL-1β刺激後，C 組 NF-κB DNA 結閤活性、ICAM-1 mRNA 和蛋白明顯升高（P ＜0．01），D 組 NF-κB DNA 結閤活性、ICAM-1 mRNA 和蛋白高于 A 組（P ＜0．05），但低于 C 組（P ＜0．05），PHC 預處理能抑製 IL-1β誘導的 NF-κB DNA結閤活性、ICAM-1 mRNA 和蛋白錶達升高。結論PHC 可抑製 IL-1β誘導 A549細胞分泌 ICAM-1，其機製可能通過抑製 NF-κB 激活。
목적：탐토염산무을규미（PHC）억제백세포개소-1β（IL-1β）유도 A549세포분비세포간점부분자-1（ICAM-1）급기작용궤제。방법체외배양 A549세포주，분별용배양액（A 조）、PHC （B 조）、IL-1β（C 조）화 IL-1β＋PHC（D 조）처리，NF-κB DNA 결합활성시제합검측자격후1 h NF-κB DNA 결합활성；반전록-취합매련반응검측자격후4 h ICAM-1 mRNA 표체；매련면역흡부법검측자격후24 h ICAM-1단백표체。결과IL-1β자격후，C 조 NF-κB DNA 결합활성、ICAM-1 mRNA 화단백명현승고（P ＜0．01），D 조 NF-κB DNA 결합활성、ICAM-1 mRNA 화단백고우 A 조（P ＜0．05），단저우 C 조（P ＜0．05），PHC 예처리능억제 IL-1β유도적 NF-κB DNA결합활성、ICAM-1 mRNA 화단백표체승고。결론PHC 가억제 IL-1β유도 A549세포분비 ICAM-1，기궤제가능통과억제 NF-κB 격활。
Objective To investigate the inhibitory of penehycldine hydrochloride (PHC) on interleukin-1β(IL-1β)-induced intercellular adhesion molecule -1 (ICAM-1) in A549 cells and its mechanism.Methods A549 cells were cultured in vitro and treated with cell culture medium (group A),PHC(group B),IL-1β(group C) and IL-1β+PHC(group D),respectively.The DNA binding activity of nuclear factor-κB(NF-κB) was detected 1 hour after IL-1βtreatment according to the kit.The expression of ICAM-1 mRNA was detected by using reverse transcriptase-polymerase chain reaction(RT-PCR) 4 hours after stimulation.The expression of ICAM-1 protein was detected by using enzyme-linked immunosorbent assay(ELISA) 24 hours after stimulation.Results After IL-1βstimulation,the DNA binding activity of NF-κB,the expressions of ICAM-1 mRNA and ICAM-1 protein increased significantly in group C(P <0.01),which in group D were higher than those in group A(P <0.05) but lower than those in group C(P <0.05),PHC could inhibit the DNA binding activity of NF-κB induced by IL-1β,and the expressions of ICAM-1 mRNA and protein increased.Conclusion PHC might inhibit IL-1β-induced ICAM-1 in A549 cells by suppressing the activation of NF-κB.
