LZ205, a newly synthesized flavonoid compound, exerts anti-inflammatory effect by inhibiting M1 macrophage polarization through regulating PI3K/AKT/mTOR signaling pathway
LZ205, a newly synthesized flavonoid compound, exerts anti-inflammatory effect by inhibiting M1 macrophage polarization through regulating PI3K/AKT/mTOR signaling pathway
复制标题
新合成的黄酮类化合物LZ205通过调节PI3K/AKT/mTOR信号通路抑制M1巨噬细胞极化发挥抗炎作用
DOI：
10.1016/j.yexcr.2018.01.033
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发表时间：
2018-03-01
影响因子：
3.7
通讯作者：
Lu, Na
中科院分区：
文献类型：
--
作者：
Bai, Dongsheng;Zhao, Yue;Lu, Na
巨噬细胞极化参与炎症过程。调节巨噬细胞极化被认为是治疗各种炎症性疾病的有效方法。在我们的研究中，我们研究了具有抗炎特性的黄酮类化合物LZ 205的潜在分子机制。结果显示，LZ 205通过调节PI 3 K/AKT/mTOR信号通路，显著降低M1巨噬细胞相关促炎细胞因子的分泌，而不影响M2巨噬细胞相关细胞因子的mRNA水平。体内研究表明，12205显著抑制DSS诱导的结肠炎和明矾诱导的小鼠腹膜炎中的M1巨噬细胞极化。与体外研究一致，LZ 205显著阻断结肠组织和腹膜巨噬细胞中PI 3 K、p-AKT和p-mTOR的表达。总之，LZ 205通过调节PI 3 K/AKT/mTOR信号通路抑制M1巨噬细胞极化而发挥抗炎作用。
Macrophage polarization is involved in the process of inflammation. Regulation of macrophage polarization is considered to be an effective method for the treatment of various inflammatory diseases. In our study, we investigated the potential molecular mechanism of the flavonoid compound LZ205, which exhibits anti-inflammatory property. Results showed that LZ205 significantly reduced M1 macrophage-associated proin-flammatory cytokines secretion by regulating PI3K/AKT/mTOR signaling pathway without affecting M2 macrophage-associated cytokines mRNA levels. In vivo studies showed that 12205 significantly inhibited M1 macrophages polarization in DSS-induced colitis and alum-induced murine peritonitis. Consistent with in vitro studies, LZ205 significantly blocked expression of PI3K, p-AKT and p-mTOR in colon tissues and peritoneal macrophages. Taken together, LZ205 exerts anti-inflammatory effect by inhibiting M1 macrophage polarization via regulating PI3K/AKT/mTOR signaling pathway.