基础医学与临床 ›› 2018, Vol. 38 ›› Issue (12): 1749-1752.

• 研究论文 • 上一篇    下一篇

脂氧素A4降低LPS致肥胖大鼠炎性因子的释放

吴铭1,蒋苇苇2,高莉莉1   

  1. 1. 徐州医科大学附属医院
    2. 徐州医科大学
  • 收稿日期:2018-05-08 修回日期:2018-07-23 出版日期:2018-12-05 发布日期:2018-11-23
  • 通讯作者: 高莉莉 E-mail:14083054@qq.com

LXA4 reduces LPS-induced inflammatory cytokines release in obesity rats

  • Received:2018-05-08 Revised:2018-07-23 Online:2018-12-05 Published:2018-11-23

摘要: 目的 探讨脂氧素A4对LPS致肥胖大鼠炎性因子释放的影响 方法 将大鼠分为普通饲料(ND)及高脂饲料(HFD)喂养组,再将2组大鼠分成对照组、LPS(脂多糖)组及LXA4(脂氧素A4)干预组。12 h后处死,心脏取血留取血清, ELISA检测血清TNFα及IL-6水平。Western blot检测肝组织NF-κB及MAPK下游信号通路的活化。结果HFD组较ND组大鼠IL-6和TNFα的释放量明显增加(P<0.05);LPS可致ND及HFD组IL-6及TNFα的释放明显增加(P<0.05),而使用LXA4干预后可以明显降低IL-6及TNFα的释放(P<0.05)。HFD较ND组大鼠的NF-kB及MAPK信号通路明显活化;LXA4的干预可降低LPS致ND及HFD组NF-kB及MAPK信号通路的活化。结论 LXA4干预能够有效降低LPS致肥胖大鼠炎性因子的释放,并可抑制NF-kB及MAPK下游信号通路的活化,对肥胖及炎性反应有双重保护作用。

关键词: 脂氧素A4, 肥胖, 脓毒症

Abstract: Objective To study the effects of LXA4 to the releasing of inflammatory cytokines in obese rat. Methods Rats were used to create obesity model with high fat diet (HFD) and the control group were fed with normal diet (ND). These successfully established models were then divided into three subgroups, including the control group, LPS group and LXA4 intervention group. All of rats were killed after 12 hours and heart blood was collected to detect TNFα and IL-6 levels though ELISA. Western Blot experiments tested the activation in the downstream NF-kB and MAPK signaling pathways. Results Comparing with ND group, IL-6 and TNFα levels both increased significantly in HFD group(P<0.05). After LPS injection, the levels of IL-6 and TNFα both increased in ND and HFD group(P<0.05). However, LXA4 intervention can obviously decrease the releasing of IL-6 and TNFα(P<0.05). Both NF-kB and MAPK signaling pathways activated obviously in HFD group comparing with ND group. In addition, LXA4 intervention can decrease the activation of NF-kB and MAPK signaling pathways caused by LPS in ND and HFD group. Conclusion LXA4 intervention can effectively reduce the serum levels of inflammatory cytokines and inhibit the activation of NF-kB and MAPK signaling pathways caused by LPS in obese rats, which revealing dual protective effects on obesity and inflammatory reaction.

Key words: LXA4, obesity, sepsis

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