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Anti-inflammatory effect of hispidin on LPS induced macrophage inflammation through MAPK and JAK1/STAT3 signaling pathways
Applied Biological Chemistry ( IF 2.3 ) Pub Date : 2020-05-04 , DOI: 10.1186/s13765-020-00504-2
Ying-Hao Han , Dong-Qin Chen , Mei-Hua Jin , Ying-Hua Jin , Jing Li , Gui-Nan Shen , Wei-Long Li , Yi-Xi Gong , Ying-Ying Mao , Dan-Ping Xie , Dong-Seok Lee , Li-Yun Yu , Sun-Uk Kim , Ji-Su Kim , Taeho Kwon , Yu-Dong Cui , Hu-Nan Sun

Severe inflammatory reactions caused by macrophage activation can trigger a systemic immune response. In the present study, we observed the anti-inflammatory properties of hispidin on LPS induced RAW264.7 macrophage cells. Our results showed that hispidin treatment significantly reduced the production of cellular NO, IL-6 and reactive oxygen species (ROS) while has not inhibitory effect on TNF-α productions. Excitingly, hispidin treatment retains the phagocytosis ability of macrophages which enabling them to perform the function of removing foreign invaders. Signaling studies showed, hispidin treatment dramatic suppressed the LPS induced mitogen activated protein kinases (MAPK) and JAK/STAT activations. In conclusion, our findings suggest that hispidin may be a new therapeutic target for clinical treatment of macrophages-mediated inflammatory responses.

中文翻译:

Hispidin通过MAPK和JAK1 / STAT3信号通路对LPS诱导的巨噬细胞炎症的抗炎作用

巨噬细胞活化引起的严重炎症反应可引发全身性免疫反应。在本研究中,我们观察到了组氨酸对LPS诱导的RAW264.7巨噬细胞的抗炎特性。我们的结果表明,组氨酸治疗显着降低了细胞NO,IL-6和活性氧(ROS)的产生,而对TNF-α的产生没有抑制作用。令人兴奋的是,组蛋白治疗保留了巨噬细胞的吞噬能力,​​使它们能够执行清除外来入侵者的功能。信号研究表明,组蛋白治疗显着抑制了LPS诱导的丝裂原活化蛋白激酶(MAPK)和JAK / STAT活化。结论,
更新日期:2020-05-04
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