中华微生物学和免疫学杂志
中華微生物學和免疫學雜誌
중화미생물학화면역학잡지
Chinese Journal of Microbiology and Immunology
2015年
7期
502-505
,共4页
小鼠肺泡巨噬细胞%腺苷酸活化蛋白激酶%脂多糖%炎症因子
小鼠肺泡巨噬細胞%腺苷痠活化蛋白激酶%脂多糖%炎癥因子
소서폐포거서세포%선감산활화단백격매%지다당%염증인자
Mice alveolar macrophage%Adenosine monophosphate-activated protein kinase%LPS%Inflammatory cytokine
目的 探讨腺苷酸活化蛋白激酶( AMP-activated protein kinase, AMPK)在小鼠肺泡巨噬细胞由脂多糖( lipopolysaccharide,LPS)诱导炎症因子分泌中的作用机制. 方法 选择野生型和AMPKα1-/-小鼠原代肺泡巨噬细胞,ELISA(酶联免疫吸附剂测定)方法检测在有无AMPK的激动剂[5-氨基-4-甲酰胺咪唑核糖核苷酸(5-amino-1-β-D-ribofuranosyl-imidazole-4-carboxamide,AICAR)]作用下LPS刺激的细胞上清中肿瘤坏死因子-α( TNF-α)、白细胞介素-1β( IL-1β)分泌;Western blot方法检测AMPKα1、α2在野生型和AMPKα1-/-小鼠肺泡巨噬细胞中的表达, LPS作用下p-AMPKα活性变化. 结果 AMPKα1-/-小鼠肺泡巨噬细胞中LPS刺激的炎症因子分泌显著高于野生型;野生型小鼠肺泡巨噬细胞LPS下调p-AMPKα活性, AICAR显著抑制LPS诱导的TNF-α、IL-1β的分泌. 结论AMPKα1缺失促进了LPS诱导的炎症因子分泌,AMPK激动剂AICAR显著抑制LPS诱导的炎症因子分泌,AMPK参与了小鼠肺泡巨噬细胞中内毒素诱导的炎症因子分泌调控.
目的 探討腺苷痠活化蛋白激酶( AMP-activated protein kinase, AMPK)在小鼠肺泡巨噬細胞由脂多糖( lipopolysaccharide,LPS)誘導炎癥因子分泌中的作用機製. 方法 選擇野生型和AMPKα1-/-小鼠原代肺泡巨噬細胞,ELISA(酶聯免疫吸附劑測定)方法檢測在有無AMPK的激動劑[5-氨基-4-甲酰胺咪唑覈糖覈苷痠(5-amino-1-β-D-ribofuranosyl-imidazole-4-carboxamide,AICAR)]作用下LPS刺激的細胞上清中腫瘤壞死因子-α( TNF-α)、白細胞介素-1β( IL-1β)分泌;Western blot方法檢測AMPKα1、α2在野生型和AMPKα1-/-小鼠肺泡巨噬細胞中的錶達, LPS作用下p-AMPKα活性變化. 結果 AMPKα1-/-小鼠肺泡巨噬細胞中LPS刺激的炎癥因子分泌顯著高于野生型;野生型小鼠肺泡巨噬細胞LPS下調p-AMPKα活性, AICAR顯著抑製LPS誘導的TNF-α、IL-1β的分泌. 結論AMPKα1缺失促進瞭LPS誘導的炎癥因子分泌,AMPK激動劑AICAR顯著抑製LPS誘導的炎癥因子分泌,AMPK參與瞭小鼠肺泡巨噬細胞中內毒素誘導的炎癥因子分泌調控.
목적 탐토선감산활화단백격매( AMP-activated protein kinase, AMPK)재소서폐포거서세포유지다당( lipopolysaccharide,LPS)유도염증인자분비중적작용궤제. 방법 선택야생형화AMPKα1-/-소서원대폐포거서세포,ELISA(매련면역흡부제측정)방법검측재유무AMPK적격동제[5-안기-4-갑선알미서핵당핵감산(5-amino-1-β-D-ribofuranosyl-imidazole-4-carboxamide,AICAR)]작용하LPS자격적세포상청중종류배사인자-α( TNF-α)、백세포개소-1β( IL-1β)분비;Western blot방법검측AMPKα1、α2재야생형화AMPKα1-/-소서폐포거서세포중적표체, LPS작용하p-AMPKα활성변화. 결과 AMPKα1-/-소서폐포거서세포중LPS자격적염증인자분비현저고우야생형;야생형소서폐포거서세포LPS하조p-AMPKα활성, AICAR현저억제LPS유도적TNF-α、IL-1β적분비. 결론AMPKα1결실촉진료LPS유도적염증인자분비,AMPK격동제AICAR현저억제LPS유도적염증인자분비,AMPK삼여료소서폐포거서세포중내독소유도적염증인자분비조공.
Objective To investigate the mechanism of 5′adenosine monophosphate-activated pro-tein kinase ( AMPK) in the regulation of LPS-induced secretion of inflammatory cytokines in mouse alveolar macrophages.Methods Alveolar macrophages were isolated from wild type and AMPKα1-/-C57BL/6J mice.ELISA was used to measure the concentrations of IL-1βand TNF-αin the culture supernatants of LPS treated alveolar macrophages with or without 5-amino-1-β-D-ribofuranosyl-imidazole-4-carboxamide ( AICAR ) stimulation.Western blot assay was performed to analyze the expression of AMPKα1 and AMPKα2 in alveolar macrophages isolated from wild type and AMPKα1-/-mice as well as the LPS-induced changes of p-AMPKαactivity in wild type mice.Results The LPS-induced secretion of inflammatory cyto-kines in alveolar macrophages isolated from AMPKα1-/-mice were significantly higher than that of wild type mice.The activities of p-AMPKαin wild type mice were suppressed by LPS treatment.Treatment of AICAR inhibited the LPS-induced secretion of TNF-αand IL-1β.Conclusion The LPS-induced secretion of in-flammatory cytokines was enhanced in AMPKα1-deficient mice, but could be suppressed upon the treatment of AICAR, an agonist of AMPK.AMPK was involved in the regulation of LPS-induced secretion of inflamma-tory cytokines by alveolar macrophages in mice.