中国急救医学
中國急救醫學
중국급구의학
Chinese Journal of Critical Care Medicine
2015年
11期
1044-1047
,共4页
徐亚杰%鲍红光%王晓亮%斯妍娜%孙凡%潘笑笑
徐亞傑%鮑紅光%王曉亮%斯妍娜%孫凡%潘笑笑
서아걸%포홍광%왕효량%사연나%손범%반소소
脂多糖(LPS)%脂联素%AMPK%小鼠腹腔巨噬细胞
脂多糖(LPS)%脂聯素%AMPK%小鼠腹腔巨噬細胞
지다당(LPS)%지련소%AMPK%소서복강거서세포
Lipopolysaccharide ( LPS)%Adiponectin%AMPK%Mouse peritoneal macrophages
目的 探讨脂联素是否通过AMPK通路介导线粒体自噬调控炎症反应. 方法 小鼠腹腔巨噬细胞细胞分为五组:空白对照组(A组)、脂多糖组(B组)、脂联素预处理组(C组)、脂联素预处理+AMPK拮抗剂组( D组)及AMPK拮抗剂组( E组). 细胞接种于60 mm培养皿中,分别予以培基,LPS,APN联合LPS, LPS、APN联合AMPK拮抗剂Compound C,LPS联合Compound C孵育,Western blot法测定AMPK及LC3B蛋白含量,酶联免疫吸附试验(ELISA)检测 IL-1β及IL-6水平. 结果 与A组比较,B组AMPK及LC3B蛋白含量、IL-1β及IL-6水平增加( P<0.05);与B组比较,C组AMPK及LC3B蛋白含量升高(P<0.05),IL-1β及IL-6 水平降低(P<0.05);与C组比较,D组AMPK及LC3B蛋白含量降低,IL-1β及IL-6 水平升高(P<0.05 ). 结论 脂联素可调控LPS介导的炎症反应,其机制可能与激活AMPK通路、增强线粒体自噬有关.
目的 探討脂聯素是否通過AMPK通路介導線粒體自噬調控炎癥反應. 方法 小鼠腹腔巨噬細胞細胞分為五組:空白對照組(A組)、脂多糖組(B組)、脂聯素預處理組(C組)、脂聯素預處理+AMPK拮抗劑組( D組)及AMPK拮抗劑組( E組). 細胞接種于60 mm培養皿中,分彆予以培基,LPS,APN聯閤LPS, LPS、APN聯閤AMPK拮抗劑Compound C,LPS聯閤Compound C孵育,Western blot法測定AMPK及LC3B蛋白含量,酶聯免疫吸附試驗(ELISA)檢測 IL-1β及IL-6水平. 結果 與A組比較,B組AMPK及LC3B蛋白含量、IL-1β及IL-6水平增加( P<0.05);與B組比較,C組AMPK及LC3B蛋白含量升高(P<0.05),IL-1β及IL-6 水平降低(P<0.05);與C組比較,D組AMPK及LC3B蛋白含量降低,IL-1β及IL-6 水平升高(P<0.05 ). 結論 脂聯素可調控LPS介導的炎癥反應,其機製可能與激活AMPK通路、增彊線粒體自噬有關.
목적 탐토지련소시부통과AMPK통로개도선립체자서조공염증반응. 방법 소서복강거서세포세포분위오조:공백대조조(A조)、지다당조(B조)、지련소예처리조(C조)、지련소예처리+AMPK길항제조( D조)급AMPK길항제조( E조). 세포접충우60 mm배양명중,분별여이배기,LPS,APN연합LPS, LPS、APN연합AMPK길항제Compound C,LPS연합Compound C부육,Western blot법측정AMPK급LC3B단백함량,매련면역흡부시험(ELISA)검측 IL-1β급IL-6수평. 결과 여A조비교,B조AMPK급LC3B단백함량、IL-1β급IL-6수평증가( P<0.05);여B조비교,C조AMPK급LC3B단백함량승고(P<0.05),IL-1β급IL-6 수평강저(P<0.05);여C조비교,D조AMPK급LC3B단백함량강저,IL-1β급IL-6 수평승고(P<0.05 ). 결론 지련소가조공LPS개도적염증반응,기궤제가능여격활AMPK통로、증강선립체자서유관.
Objective To investigate whether adiponectin would mediate inflammation by regulating mitochondrial autophagy through AMPK pathway .Methods Mouse peritoneal macrophages were divided into five groups: control group ( C group ) , model group ( LPS group ) , Adiponectin pretreatment group (APN group), Adiponectin-pretreatment+AMPK antagonist group (D group) and AMPK antagonist group (Compound C group).Peritoneal macrophages were cultured in 60 mm dishes, treated with LPS, APN preconditioning followed by LPS , AMPK antagonist Compound C preconditioning followed by APN and LPS , and Compound C preconditioning followed by LPS .Western blot method was used to determine the content of AMPK and LC3B, enzyme-linked immune adsorption assay (ELISA) was used to detect the level of IL -1 beta and IL -6.Results Compared with C group , AMPK and LC3B protein content in LPS group increased significantly , also the level of IL -1 beta and IL -6 showed an increase (P<0.05).Compared with LPS group, the level of AMPK and LC3B increased significantly, however the level of IL -1βand IL -6 showed a decrease in APN group (P<0.05). Compared with APN group , the level of AMPK and LC3B were decreased , and level of IL-1βand IL-6 showed an increase in D group .Conclusion Adiponectin may regulate the inflammatory response mediated by LPS , and its mechanism may be related to the activation of AMPK pathway and the enhancement of autophagy .