中华航海医学与高气压医学杂志
中華航海醫學與高氣壓醫學雜誌
중화항해의학여고기압의학잡지
CHINESE JOURNAL OF NAUTICAL MEDICINE AND HYPERBARIC MEDICINE
2013年
6期
372-376
,共5页
王明科%陈双红%徐雄利%武文斌%巴剑波%陶永华
王明科%陳雙紅%徐雄利%武文斌%巴劍波%陶永華
왕명과%진쌍홍%서웅리%무문빈%파검파%도영화
脂多糖%人支气管上皮细胞%环氧化酶-2%SB203580
脂多糖%人支氣管上皮細胞%環氧化酶-2%SB203580
지다당%인지기관상피세포%배양화매-2%SB203580
Lipopolysaccharide%Human bronchial epithelial cells%Cycloxygenase-2%SB203580
目的 探讨脂多糖对人支气管上皮BEAS-2B细胞环氧化酶-2(cycloxygenase-2,COX-2)表达的影响及p38丝裂原活化蛋白激酶(p38 mitogen-activated protein kinase,p38 MAPK)信号通路在其中的作用.方法 用0、0.1、1、10、100 mg/L脂多糖(lipopolysaccharide,LPS)处理人支气管上皮BEAS-2B细胞2h,逆转录-聚合酶链反应(reverse transcription-polymerase chain reaction,RT-PCR)检测COX-2的表达进行量效实验.用10 mg/L LPS处理人支气管上皮BEAS-2B细胞0、2、6、12、24 h,RT-PCR检测COX-2的表达进行时效实验.最后,加入20 μmol/L SB203580(p38 MAPK抑制剂)预处理1h,再以10mg/L LPS处理人支气管上皮BEAS-2B细胞2h,RT-PCR观察SB203580对其的影响.结果 不同浓度LPS刺激BEAS-2B细胞2h后,COX-2表达随浓度增加有增加趋势,呈浓度依赖性.10 mg/L LPS刺激BEAS-2B细胞2h后,COX-2表达达到高峰,之后降低,24 h降到基础水平,与对照组比较差异无统计学意义(P<0.05.).p38 MAPK抑制剂SB203580可部分抑制LPS诱导BEAS-2B细胞COX-2的表达.结论 LPS浓度依赖性诱导人支气管上皮BEAS-2B细胞COX-2表达增加,2h为表达高峰.p38 MAPK参与了调控LPS诱导BEAS-2B细胞COX-2的表达.
目的 探討脂多糖對人支氣管上皮BEAS-2B細胞環氧化酶-2(cycloxygenase-2,COX-2)錶達的影響及p38絲裂原活化蛋白激酶(p38 mitogen-activated protein kinase,p38 MAPK)信號通路在其中的作用.方法 用0、0.1、1、10、100 mg/L脂多糖(lipopolysaccharide,LPS)處理人支氣管上皮BEAS-2B細胞2h,逆轉錄-聚閤酶鏈反應(reverse transcription-polymerase chain reaction,RT-PCR)檢測COX-2的錶達進行量效實驗.用10 mg/L LPS處理人支氣管上皮BEAS-2B細胞0、2、6、12、24 h,RT-PCR檢測COX-2的錶達進行時效實驗.最後,加入20 μmol/L SB203580(p38 MAPK抑製劑)預處理1h,再以10mg/L LPS處理人支氣管上皮BEAS-2B細胞2h,RT-PCR觀察SB203580對其的影響.結果 不同濃度LPS刺激BEAS-2B細胞2h後,COX-2錶達隨濃度增加有增加趨勢,呈濃度依賴性.10 mg/L LPS刺激BEAS-2B細胞2h後,COX-2錶達達到高峰,之後降低,24 h降到基礎水平,與對照組比較差異無統計學意義(P<0.05.).p38 MAPK抑製劑SB203580可部分抑製LPS誘導BEAS-2B細胞COX-2的錶達.結論 LPS濃度依賴性誘導人支氣管上皮BEAS-2B細胞COX-2錶達增加,2h為錶達高峰.p38 MAPK參與瞭調控LPS誘導BEAS-2B細胞COX-2的錶達.
목적 탐토지다당대인지기관상피BEAS-2B세포배양화매-2(cycloxygenase-2,COX-2)표체적영향급p38사렬원활화단백격매(p38 mitogen-activated protein kinase,p38 MAPK)신호통로재기중적작용.방법 용0、0.1、1、10、100 mg/L지다당(lipopolysaccharide,LPS)처리인지기관상피BEAS-2B세포2h,역전록-취합매련반응(reverse transcription-polymerase chain reaction,RT-PCR)검측COX-2적표체진행량효실험.용10 mg/L LPS처리인지기관상피BEAS-2B세포0、2、6、12、24 h,RT-PCR검측COX-2적표체진행시효실험.최후,가입20 μmol/L SB203580(p38 MAPK억제제)예처리1h,재이10mg/L LPS처리인지기관상피BEAS-2B세포2h,RT-PCR관찰SB203580대기적영향.결과 불동농도LPS자격BEAS-2B세포2h후,COX-2표체수농도증가유증가추세,정농도의뢰성.10 mg/L LPS자격BEAS-2B세포2h후,COX-2표체체도고봉,지후강저,24 h강도기출수평,여대조조비교차이무통계학의의(P<0.05.).p38 MAPK억제제SB203580가부분억제LPS유도BEAS-2B세포COX-2적표체.결론 LPS농도의뢰성유도인지기관상피BEAS-2B세포COX-2표체증가,2h위표체고봉.p38 MAPK삼여료조공LPS유도BEAS-2B세포COX-2적표체.
Objective To investigate the effect of lipopolysaccharide (LPS) on the expression of cycloxygenase-2 (COX-2) in human bronchial epithelial cells (BEAS-2B),and the role of p38 mitogen-activated protein kinase (MAPK) signal pathway in the expression of COX-2 induced by LPS.Methods Human BEAS2B cells were treated for 2 hours with different concentrations of LPS (0,0.1,1,10,100 mg/L),and the expression levels of COX-2 were monitored with RT-PCR and dose-effect experiment was performed accordingly.Human BEAS-2B cells were treated with 10 mg/L LPS for 0,2,6,12 and 24 hours,and the expression levels of COX-2 were monitored with RT-PCR and dose-effect experiment was also performed.BEAS-2B cells were pretreated with 20 μmol/L SB203580 (p38 MAPK inhibitor) for 1 hour,and then exposed to 10 mg/L LPS for 2 hours.Effect of SB203580 on the expression of COX-2 was detected with RT-PCR.Results COX-2 expression tended to increase,when different concentrations of LPS treated BEAS-2B cells for 2 hours,with the expression level being obviously dose-dependent.After BEAS-2B cells were treated for 2 hours with 10 mg/L LPS,COX-2 expression reached peak,then decreased,and finally came to the basal level at 24 h.And no statistical significance could be noted,when it was compared with that of the control group (P < O.05).p38 MAPK inhibitor,SB203580,could partially inhibit COX-2 expression induced by LPS in BEAS-2B cells.Conclusions LPS could induce the COX-2 expression in BEAS-2B cells in a dose-dependent manner,and the COX-2 expression reaches the peak at 2 h.p38 MAPK is involved in the COX-2 expression induced by LPS in BEAS-2B cells.