| 崔敏萱,王文文,向 安,杨 媛,卢兹凡,汪 莉.线粒体来源肽MOTS-c通过抑制促炎性因子分泌改善脓毒症小鼠生存率[J].,2019,19(15):2839-2844 |
| 线粒体来源肽MOTS-c通过抑制促炎性因子分泌改善脓毒症小鼠生存率 |
| Mitochondrial-derived Peptide MOTS-c Improves Survival in Septic Mice Via Reducing Pro-inflammatory Cytokine Production |
| 投稿时间：2019-01-26 修订日期：2019-02-22 |
| DOI：10.13241/j.cnki.pmb.2019.15.008 |
| 中文关键词: 线粒体来源肽 MOTS-c 脓毒症 |
| 英文关键词: Mitochondrial-derived peptide MOTS-c Sepsis |
| 基金项目:国家肿瘤重点实验室自主课题（CBSKL2017Z18） |
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| 中文摘要: |
| 摘要 目的：研究一种新的线粒体来源肽MOTS-c对脓毒症小鼠生存率的影响。方法：构建了LPS和CLP诱导的两种脓毒症小鼠模型，观察MOTS-c治疗对小鼠生存率及促炎性因子TNF-α和IL-6水平的影响。Western-blot方法检测MOTS-c对巨噬细胞NF-κB活化的影响。结果：与对照组相比，MOTS-c治疗使LPS诱导的脓毒症小鼠生存率从10%提高至60% （P<0.05），而CLP诱导的脓毒症小鼠生存率则从10%提高至50% （P<0.05）。ELISA结果显示，在LPS诱导的脓毒症模型中，MOTS-c治疗使小鼠血浆中的TNF-α和IL-6的水平显著降低（P<0.05）；与之类似，在CLP诱导的脓毒症模型中，小鼠血浆和腹腔灌洗液中的TNF-α和IL-6的水平也显著下降（P<0.05）。机制研究结果表明，MOTS-c能够显著抑制巨噬细胞中LPS诱导的转录因子NF-κB的活化。结论：MOTS-c能够提高脓毒症小鼠的生存率，其机制可能与抑制NF-κB的转录激活、降低体内促炎性细胞因子的水平相关。 |
| 英文摘要: |
| ABSTRACT Objective: This study aimsto explore the effects of a mitochondrial-derived peptide MOTS-c treatmenton survival in septic mice. Methods: Two models of sepsis were constructed, one due to lipopolysaccharide (LPS) and the other to cecal ligation and puncture (CLP). The survival rate and pro-inflammatory cytokine levels were detected and compared in septic mice. The influence of MOTS-c on LPS-induced NF-κB activation in macrophages was also analyzed by western-blot. Results: Compared to control group, MOTS-c treatment increased the mice survival rate from 10% to 60% in LPS-induced model（P<0.05）, and from 10% to 50% in CLP-induced sepsis （P<0.05）separately. The levels of TNF-α and IL-6 in mice blood plasm were decreased in both two septic models by ELISA analysis. Moreover, MOTS-c treatment reduced the TNF-α and IL-6 concentration in peritoneal fluid of CLP-induced septic mice（P<0.05）. Mechanically, the NF-αB activation was suppressed by MOTS-c in LPS challenged macrophages. Conclusion: Our data indicated that MOTS-c could inhibit the activation of NF-κB and suppress the expression of pro-inflammatory cytokines, thus leading to increased survival in septic mice. |
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