中华临床医师杂志(电子版)
中華臨床醫師雜誌(電子版)
중화림상의사잡지(전자판)
CHINESE JOURNAL OF CLINICIANS(ELECTRONIC VERSION)
2013年
3期
1129-1133
,共5页
鲍红光%徐丽%沈妍%刘晨辉%蔡朦朦%杨建平
鮑紅光%徐麗%瀋妍%劉晨輝%蔡朦朦%楊建平
포홍광%서려%침연%류신휘%채몽몽%양건평
脂联素%脓毒症%白细胞介素6%转录激活因子3%肺损伤
脂聯素%膿毒癥%白細胞介素6%轉錄激活因子3%肺損傷
지련소%농독증%백세포개소6%전록격활인자3%폐손상
Adiponectin%Sepsis%Interleukin-6%Activating transcription factor 3%Lung injury
目的研究脂联素(APN)对脓毒症大鼠肺组织白细胞介素-6(IL-6)/信号转导及转录激活因子3(STAT3)通路的影响。方法盲肠结扎穿孔(CLP)法制作脓毒症动物模型,雄性Wistar大鼠120只,10~14周龄,体重250~300 g,随机分为对照组( C组)、脓毒症模型组( CLP组)和脂联素预处理组( APN组),分别于术后2 h、6 h、12 h、24 h、48 h处死,采用酶联免疫吸附法(ELISA)检测肺组织匀浆中IL-6表达水平,半定量逆转录聚合酶链反应( RT-PCR)法检测肺组织匀浆中IL-6 mRNA的表达水平;凝胶阻滞电泳分析技术( EMSA)检测肺组织STAT3的DNA结合活性;同时检测肺组织髓过氧化物酶( MPO)活性;各组剩余10只大鼠观察术后7 d的生存率,并绘制生存曲线。结果与C组比较,CLP组大鼠肺组织IL-6 mRNA及蛋白表达水平升高,STAT3的DNA结合活性表达升高,肺组织匀浆中MPO活性显著升高,死亡率升高( P均<0.05);与CLP组比较,APN组大鼠肺组织IL-6 mRNA及蛋白表达水平下降,STAT3的DNA结合活性表达降低,肺组织匀浆中MPO活性显著下降,死亡率明显降低( P均<0.05)。结论脂联素可能通过抑制IL-6/STAT3信号转导通路,从而减轻脓毒症性肺损伤。
目的研究脂聯素(APN)對膿毒癥大鼠肺組織白細胞介素-6(IL-6)/信號轉導及轉錄激活因子3(STAT3)通路的影響。方法盲腸結扎穿孔(CLP)法製作膿毒癥動物模型,雄性Wistar大鼠120隻,10~14週齡,體重250~300 g,隨機分為對照組( C組)、膿毒癥模型組( CLP組)和脂聯素預處理組( APN組),分彆于術後2 h、6 h、12 h、24 h、48 h處死,採用酶聯免疫吸附法(ELISA)檢測肺組織勻漿中IL-6錶達水平,半定量逆轉錄聚閤酶鏈反應( RT-PCR)法檢測肺組織勻漿中IL-6 mRNA的錶達水平;凝膠阻滯電泳分析技術( EMSA)檢測肺組織STAT3的DNA結閤活性;同時檢測肺組織髓過氧化物酶( MPO)活性;各組剩餘10隻大鼠觀察術後7 d的生存率,併繪製生存麯線。結果與C組比較,CLP組大鼠肺組織IL-6 mRNA及蛋白錶達水平升高,STAT3的DNA結閤活性錶達升高,肺組織勻漿中MPO活性顯著升高,死亡率升高( P均<0.05);與CLP組比較,APN組大鼠肺組織IL-6 mRNA及蛋白錶達水平下降,STAT3的DNA結閤活性錶達降低,肺組織勻漿中MPO活性顯著下降,死亡率明顯降低( P均<0.05)。結論脂聯素可能通過抑製IL-6/STAT3信號轉導通路,從而減輕膿毒癥性肺損傷。
목적연구지련소(APN)대농독증대서폐조직백세포개소-6(IL-6)/신호전도급전록격활인자3(STAT3)통로적영향。방법맹장결찰천공(CLP)법제작농독증동물모형,웅성Wistar대서120지,10~14주령,체중250~300 g,수궤분위대조조( C조)、농독증모형조( CLP조)화지련소예처리조( APN조),분별우술후2 h、6 h、12 h、24 h、48 h처사,채용매련면역흡부법(ELISA)검측폐조직균장중IL-6표체수평,반정량역전록취합매련반응( RT-PCR)법검측폐조직균장중IL-6 mRNA적표체수평;응효조체전영분석기술( EMSA)검측폐조직STAT3적DNA결합활성;동시검측폐조직수과양화물매( MPO)활성;각조잉여10지대서관찰술후7 d적생존솔,병회제생존곡선。결과여C조비교,CLP조대서폐조직IL-6 mRNA급단백표체수평승고,STAT3적DNA결합활성표체승고,폐조직균장중MPO활성현저승고,사망솔승고( P균<0.05);여CLP조비교,APN조대서폐조직IL-6 mRNA급단백표체수평하강,STAT3적DNA결합활성표체강저,폐조직균장중MPO활성현저하강,사망솔명현강저( P균<0.05)。결론지련소가능통과억제IL-6/STAT3신호전도통로,종이감경농독증성폐손상。
Objective To investigate the effect of adiponectin ( APN) on interlukin-6 and signal transducer and activator of transcription 3(STAT3)in rats with sepsis.Methods The animal model of sepsis was established by ceal ligation and puncture(CLP)in 120 Wistar male rats(weighting 250-300 g,at the age of 10-14 weeks old),which were randomly divided into 3 groups:control group ( C group ) , CLP group and adiponectin treatment group ( APN group).At 2,6,12,24,48 h after CLP,IL-6 concentration in lung homogenate was detected by enzyme linked immunosorbent assay ( ELISA ) .Lung IL-6 mRNA was detected with semi-quantitative reverse transcriptase polymerase chain reaction(RT-PCR) chain reaction(real-time RT-PCR),and the DNA-binding activity of STAT3 was analyzed by electrophoretic mobility shift assay (EMSA),while the myeloperoxidase(MPO)activity in lung tissue was determined.The mortality rate was calculated 7 d after operation and the survival curves were drawn . Results Compared with C group,gene and protein expression of IL-6 in group CLP was increased,and the DNA-binding activity of STAT3 and MPO activity in lung homogenate was raised ,as well as the mortality rate (all P<0.05 ) .Compared with CLP group , gene and protein expression of IL-6 in group APN was decreased , DNA-binding activity of STAT3 and MPO activity in lung homogenate was lower , as well as the mortality rate ( all P <0.05 ) . Conclusions APN may attenuate lung injury in CLP-induced septic rats through inhibiting the IL-6/STAT3 signaling pathway .