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N-阿魏酰基血清素通过 SIRT1 刺激的 FOXO1 和 NF-κB 信号通路抑制 RAW 264.7 细胞中的脂多糖诱导的炎症。

N-Feruloylserotonin inhibits lipopolysaccharide-induced inflammation via SIRT1-stimulated FOXO1 and NF-κB signaling pathways in RAW 264.7 cells.

机构信息

Institute of New Frontier Research Team, Research Institute of Medical-Bio Convergence, Hallym University, Chuncheon 24252, Republic of Korea.

Department of Food and Life Science, Pukyong National University, Busan 48513, Republic of Korea.

出版信息

Cell Mol Biol (Noisy-le-grand). 2023 Nov 15;69(11):109-115. doi: 10.14715/cmb/2023.69.11.17.

DOI:10.14715/cmb/2023.69.11.17
PMID:38015533
Abstract

Macrophages become activated by a variety of stimuli such as lipopolysaccharide (LPS) and participate in the process of immune responses. Activated macrophages produce various inflammatory mediators. In the present study, we investigated the anti-inflammatory mechanism of a serotonin derivative, N-feruloylserotonin, isolated from safflower seeds in RAW 264.7 macrophages. N-Feruloylserotonin treatment significantly attenuated these effects on LPS-induced reactive oxygen species, nitric oxide, and prostaglandin E2 production in RAW 264.7 macrophages. Furthermore, N-feruloylserotonin significantly decreased the abnormal expression of mitogen-activated protein kinase, such as phosphor (p)-c-Jun N-terminal kinase and p-extracellular-signal regulated kinase activation. Further research revealed that N-feruloylserotonin could stimulate sirtuin1 (SIRT1), then promote the forkhead box protein O1 (FOXO1), and suppress nuclear factor-kappa B (NF-kB) signaling pathways. The present study suggests that N-feruloylserotonin may be a new anti-inflammatory component and a promising candidate for anti-inflammatory therapeutic agents through the regulation of SIRT1-stimulated FOXO1 and NF-kB signaling pathways.

摘要

巨噬细胞被多种刺激物如脂多糖(LPS)激活,并参与免疫反应过程。激活的巨噬细胞产生各种炎症介质。在本研究中,我们研究了从红花种子中分离出的 5-羟色胺衍生物 N-阿魏酰-5-羟色胺在 RAW 264.7 巨噬细胞中的抗炎机制。N-阿魏酰-5-羟色胺处理显著减弱了 LPS 诱导的 RAW 264.7 巨噬细胞中活性氧、一氧化氮和前列腺素 E2 产生的这些作用。此外,N-阿魏酰-5-羟色胺显著降低了丝裂原激活蛋白激酶(如磷酸化 c-Jun N 末端激酶和 p-细胞外信号调节激酶)的异常表达。进一步的研究表明,N-阿魏酰-5-羟色胺可以刺激 SIRT1(沉默信息调节因子 1),然后促进 FOXO1(叉头框蛋白 O1),并抑制核因子-κB(NF-κB)信号通路。本研究表明,N-阿魏酰-5-羟色胺可能是一种新的抗炎成分,通过调节 SIRT1 刺激的 FOXO1 和 NF-κB 信号通路,是一种有前途的抗炎治疗药物候选物。

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