...
首页> 外文期刊>Mediators of inflammation >Inhibition of P38 MAPK Downregulates the Expression of IL-1 beta to Protect Lung from Acute Injury in Intestinal Ischemia Reperfusion Rats
【24h】

Inhibition of P38 MAPK Downregulates the Expression of IL-1 beta to Protect Lung from Acute Injury in Intestinal Ischemia Reperfusion Rats

机译:P38 MAPK对P38 MAPK的抑制下调IL-1β的表达免受肠缺血再灌注大鼠急性损伤的保护肺

获取原文
获取原文并翻译 | 示例

摘要

Acute lung injury (ALI) induced by intestinal ischemia/reperfusion (II/R) has high incidence and mortality, in which IL-1 beta was essential for the full development of ALI. However, the detailed regulating mechanism for this phenomenon remains to be unclear. The purpose of this study was to investigate whether inhibition of P38 MAPK could downregulate the expression of IL-1 beta to protect lung from acute injury in II/R rats. Here, we found that the level of pulmonary edema at 16 hours after operation (hpo) was obviously enhanced compared to that in 8hpo and sham groups. Immunofluorescent staining demonstrated that IL-1 beta and P38 MAPK were detected in lung tissues. And rats with II/R have the highest translation level for IL-1 beta and phosphorylation of P38 MAPK in lung tissues at 16hpo compared with 8hpo and sham groups. Moreover, administration of SB239063, an inhibitor of P38 alpha and beta, could effectively downregulate the expressions of IL-1 beta and protects lung tissues from injury in II/R rats. Our findings indicate that the inhibition of P38 alpha and beta may downregulate the expression of IL-1 beta to protect lung from acute injury in II/R, which could be used as a potential target for reducing ALI induced by II/R in the future clinical trial.
机译:肠缺血/再灌注(II / R)诱导的急性肺损伤(ALI)具有高发病率和死亡率,其中IL-1β对ALI的全面发展是必不可少的。然而,这种现象的详细调节机制仍然不明确。本研究的目的是研究P38 MAPK的抑制是否可以下调IL-1β的表达,以保护肺免受II / R大鼠的急性损伤。在这里,与8HPO和假组相比,我们发现在术后16小时(HPO)后16小时的肺水肿水平明显增强。免疫荧光染色证明IL-1β和P38 MAPK在肺组织中检测到。与8HPO和假组相比,II / R的大鼠II / R对IL-1β和P38 MAPK的磷酸化的最高翻译水平。此外,SB239063的施用P38α和β的抑制剂可以有效地下调IL-1β的表达,并保护肺组织免受II / R大鼠的损伤。我们的研究结果表明,P38α和β的抑制可以下调IL-1β的表达,以保护肺免受II / R中的急性损伤,其可用作未来II / R诱导的ALI的潜在靶标临床试验。

著录项

  • 来源
    《Mediators of inflammation 》 |2016年第1期| 共8页
  • 作者单位

    Guizhou Prov Peoples Hosp Dept Burn &

    Plast Surg Guiyang 550002 Peoples R China;

    Kunming Med Univ Inst Neurosci Kunming 650031 Peoples R China;

    Affiliated Hosp Guiyang Med Coll Dept Pediat Guiyang 550004 Peoples R China;

    Sichuan Univ West China Hosp Translat Neurosci Ctr Inst Neurol Dis Chengdu 610041 Peoples R;

    Guizhou Prov Peoples Hosp Dept Burn &

    Plast Surg Guiyang 550002 Peoples R China;

    Guizhou Prov Peoples Hosp Dept Burn &

    Plast Surg Guiyang 550002 Peoples R China;

    Guizhou Prov Peoples Hosp Dept Burn &

    Plast Surg Guiyang 550002 Peoples R China;

    Guizhou Prov Peoples Hosp Dept Burn &

    Plast Surg Guiyang 550002 Peoples R China;

    Affiliated Hosp Guiyang Med Coll Dept Pediat Guiyang 550004 Peoples R China;

    Kunming Med Univ Inst Neurosci Kunming 650031 Peoples R China;

    Kunming Med Univ Inst Neurosci Kunming 650031 Peoples R China;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 病理学 ;
  • 关键词

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号