实用医学杂志
實用醫學雜誌
실용의학잡지
THE JOURNAL OF PRACTICAL MEDICINE
2014年
18期
2890-2893
,共4页
非诺精罗%单核细胞%LPS%抗炎%MyD88
非諾精囉%單覈細胞%LPS%抗炎%MyD88
비낙정라%단핵세포%LPS%항염%MyD88
Fenoterol%Monocyte%LPS%Anti-inflammation%Myeloid differentiation factor 88
目的：探讨β2肾上腺素受体激动剂非诺特罗（fenoterol）在单核细胞上抑制内毒素（lipopolysaccharide，LPS）诱导炎症的分子机制。方法：选择 THP-1单核细胞系，ELISA（酶联免疫吸附剂测定）方法检测在有或无 fenoterol 预先干预下，LPS 刺激的 THP-1细胞上清中炎症因子肿瘤坏死因子-α（TNF-α）、单核细胞趋化蛋白-1（MCP-1）分泌及野生型和 MyD88-/-（髓样分化因子，myeloid differentiation factor 88）小鼠腹腔巨噬细胞上清中炎症因子 TNF-α、IL-1β（白介素-1β）分泌；western blot 方法检测有或无fenoterol 预先干预下，LPS 刺激的 MyD88表达。结果：fenoterol 可以显著抑制 THP-1细胞上 LPS 诱导的MyD88的表达及 TNF-α、MCP-1的分泌和小鼠巨噬细胞 TNF-α、IL-1β的分泌，MyD88-/-小鼠腹腔巨噬细胞对 LPS 的反应显著低于野生型小鼠腹腔巨噬细胞。结论：MyD88在 LPS 诱导的炎症中发挥重要作用， fenoterol 对 LPS 诱导的 MyD88表达发挥抑制作用与其抗炎效应相关。
目的：探討β2腎上腺素受體激動劑非諾特囉（fenoterol）在單覈細胞上抑製內毒素（lipopolysaccharide，LPS）誘導炎癥的分子機製。方法：選擇 THP-1單覈細胞繫，ELISA（酶聯免疫吸附劑測定）方法檢測在有或無 fenoterol 預先榦預下，LPS 刺激的 THP-1細胞上清中炎癥因子腫瘤壞死因子-α（TNF-α）、單覈細胞趨化蛋白-1（MCP-1）分泌及野生型和 MyD88-/-（髓樣分化因子，myeloid differentiation factor 88）小鼠腹腔巨噬細胞上清中炎癥因子 TNF-α、IL-1β（白介素-1β）分泌；western blot 方法檢測有或無fenoterol 預先榦預下，LPS 刺激的 MyD88錶達。結果：fenoterol 可以顯著抑製 THP-1細胞上 LPS 誘導的MyD88的錶達及 TNF-α、MCP-1的分泌和小鼠巨噬細胞 TNF-α、IL-1β的分泌，MyD88-/-小鼠腹腔巨噬細胞對 LPS 的反應顯著低于野生型小鼠腹腔巨噬細胞。結論：MyD88在 LPS 誘導的炎癥中髮揮重要作用， fenoterol 對 LPS 誘導的 MyD88錶達髮揮抑製作用與其抗炎效應相關。
목적：탐토β2신상선소수체격동제비낙특라（fenoterol）재단핵세포상억제내독소（lipopolysaccharide，LPS）유도염증적분자궤제。방법：선택 THP-1단핵세포계，ELISA（매련면역흡부제측정）방법검측재유혹무 fenoterol 예선간예하，LPS 자격적 THP-1세포상청중염증인자종류배사인자-α（TNF-α）、단핵세포추화단백-1（MCP-1）분비급야생형화 MyD88-/-（수양분화인자，myeloid differentiation factor 88）소서복강거서세포상청중염증인자 TNF-α、IL-1β（백개소-1β）분비；western blot 방법검측유혹무fenoterol 예선간예하，LPS 자격적 MyD88표체。결과：fenoterol 가이현저억제 THP-1세포상 LPS 유도적MyD88적표체급 TNF-α、MCP-1적분비화소서거서세포 TNF-α、IL-1β적분비，MyD88-/-소서복강거서세포대 LPS 적반응현저저우야생형소서복강거서세포。결론：MyD88재 LPS 유도적염증중발휘중요작용， fenoterol 대 LPS 유도적 MyD88표체발휘억제작용여기항염효응상관。
Objective To explore the molecular mechanism of inhibition of LPS-induced inflammation by fenoterol, a β2 adrenoceptor agonist in monocyte. Methods Concentrations of interleukin 1β (IL-1β), tumor necrosis factor α (TNF-α) and MCP-1 from cell supernatants from THP-1 cells and wild type or MyD88- / - mice peritoneal macrophages stimulated by LPS in the presence or absence of fenoterol were determined by use of an ELISA system. Expression of MyD88 (myeloid differentiation factor 88) stimulated by LPS in the presence or absence of fenoterol were determined by Western blot. Results Fenoterol inhibited LPS-induced activation of MyD88 and secretion of inflammatory cytokines (TNF-α, MCP-1, and IL-1β). The reaction of MyD88- / - mice peritoneal macrophages to LPS was much lower than that of the wild type mice peritoneal macrophages. Conclusions MyD88 plays an important role in inflammation induced by LPS. The inhibition of LPS-induced expression of MyD88 by fenoterol is associated with its anti-inflammatory effect.
