苯乙基阿魏酸作为 LPS 刺激的 RAW 264.7 巨噬细胞炎症的天然抑制剂:重点关注 NF-κB、Akt 和 MAPK 信号通路。
Phenethylferulate as a natural inhibitor of inflammation in LPS-stimulated RAW 264.7 macrophages: focus on NF-κB, Akt and MAPK signaling pathways.
发表日期:2023 Nov 07
作者:
Zhongjie Yan, Yuanyu Wang, Yizhen Song, Yicong Ma, Yufan An, Ran Wen, Na Wang, Yun Huang, Xiuwen Wu
来源:
CYTOKINE & GROWTH FACTOR REVIEWS
摘要:
羌活 (NRR) 通常用于治疗炎症相关疾病。 NRR 粗品中苯乙基阿魏酸 (PF) 含量较高,但其抗炎作用尚不清楚。因此,我们旨在研究PF在脂多糖(LPS)刺激的RAW 264.7巨噬细胞中的抗炎特性及其潜在分子机制。通过MTT法测定PF对细胞活力的影响。通过使用酶联免疫吸附测定(ELISA)检测炎症介质和细胞因子的水平来研究PF的抗炎特性。此外,通过蛋白质印迹分析确定了PF的抗炎机制。PF在低于48μM的浓度下对RAW 264.7巨噬细胞没有细胞毒性。 ELISA 显示,PF 显着抑制前列腺素 E2 (PGE2)、肿瘤坏死因子 α (TNF-α)、白细胞介素 1β (IL-1β) 和白细胞介素 6 (IL-6) 的过量产生。蛋白质印迹分析表明,PF 显着抑制诱导型一氧化氮合酶 (iNOS) 和环氧合酶 2 (COX-2) 的过量产生、NF-κB 激酶 α (IκB-α)、蛋白激酶 B (Akt) 抑制剂的磷酸化、细胞外信号调节激酶 (ERK)、c-Jun N 末端激酶 (JNK) 和 p38,以及 p65 的降解和随后的核转位。PF 是作用于核因子 kappa-B (NF- LPS 刺激的 RAW 264.7 巨噬细胞中的 κB)、Akt 和丝裂原激活蛋白激酶 (MAPK) 信号通路。这项工作为 PF 作为治疗炎症介导的免疫疾病的候选药物的适用性提供了证据。© 2023。作者。
Notopterygii Rhizoma et Radix (NRR) is commonly used for the treatment of inflammation-linked diseases. Phenethylferulate (PF) is high content in NRR crude, but its anti-inflammatory effect remains unclear. Therefore, we aimed to investigate the anti-inflammatory properties of PF and its underlying molecular mechanisms in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages.The effect of PF on cell viability was measured by MTT assay. The anti-inflammatory properties of PF were studied by detecting the levels of inflammatory mediators and cytokines using enzyme-linked immunosorbent assay (ELISA). Furthermore, the anti-inflammatory mechanisms of PF were determined by Western blot analysis.PF was not cytotoxic to RAW 264.7 macrophages at the concentrations of below 48 μM. ELISA showed that PF conspicuously inhibited overproduction of prostaglandin E2 (PGE2), tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β) and interleukin 6 (IL-6). Western blot analysis showed that PF remarkably suppressed overproduction of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2), the phosphorylation of inhibitor of NF-κB kinase α (IκB-α), protein kinase B (Akt), extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinases (JNK) and p38, as well as the degradation and subsequent nuclear translocation of p65.PF is a potent inhibitor of inflammation acting on nuclear factor kappa-B (NF-κB), Akt and mitogen-activated protein kinase (MAPK) signaling pathways in LPS-stimulated RAW 264.7 macrophages. This work provides evidence for the suitability of PF as a therapeutic candidate for the management of inflammatory-mediated immune disorders.© 2023. The Author(s).