Sophora flavescens Aiton methanol extract exerts anti-inflammatory effects via reduction of Src kinase phosphorylation

Oh, Jieun; Kim, Seung A; Kwon, Ki Woong; Choi, Se Rin; Lee, Choong Hwan; Hossain, Mohammad Amjad; Kim, Eun Sil; Kim, Changmu; Lee, Byoung-Hee; Lee, Sarah; Kim, Jong-Hoon; Cho, Jae Youl

doi:10.1016/j.jep.2022.116015

Cited by 10 publications

(1 citation statement)

References 47 publications

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“…Increasing evidence has revealed that TLR4 can be activated in lipopolysaccharide (LPS)-induced macrophages, followed by stimulating the mitogen-activated protein kinase (MAPK)-and nuclear factorkappa B (NF-κB)-mediated inflammatory responses, inducing the expression of several proinflammatory cytokines and enzymes [11,12]. Several inflammatory mediators and cytokines, including nitric oxide (NO), prostaglandin E2 (PGE 2 ), interleukin-1 beta (IL-1β), and IL-6 can induce oxidative stress, which cumulatively cause lung tissue injury [13][14][15]. Therefore, repressing the biological functions of macrophages via blocking MAPK and NF-κB pathways activation may be a prospective strategy for the therapy of ALI.…”

Section: Introductionmentioning

confidence: 99%

Echinatin attenuates acute lung injury and inflammatory responses via TAK1-MAPK/NF-κB and Keap1-Nrf2-HO-1 signaling pathways in macrophages

Luo,

Wang,

Xiong

et al. 2024

PLoS ONE

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Echinatin is an active ingredient in licorice, a traditional Chinese medicine used in the treatment of inflammatory disorders. However, the protective effect and underlying mechanism of echinatin against acute lung injury (ALI) is still unclear. Herein, we aimed to explore echinatin-mediated anti-inflammatory effects on lipopolysaccharide (LPS)-stimulated ALI and its molecular mechanisms in macrophages. In vitro, echinatin markedly decreased the levels of nitric oxide (NO) and prostaglandin E2 (PGE2) in LPS-stimulated murine MH-S alveolar macrophages and RAW264.7 macrophages by suppressing inducible nitric oxide synthase and cyclooxygenase-2 (COX-2) expression. Furthermore, echinatin reduced LPS-induced mRNA expression and release of interleukin-1β (IL-1β) and IL-6 in RAW264.7 cells. Western blotting and CETSA showed that echinatin repressed LPS-induced activation of mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) pathways through targeting transforming growth factor-beta-activated kinase 1 (TAK1). Furthermore, echinatin directly interacted with Kelch-like ECH-associated protein 1 (Keap1) and activated the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway to enhance heme oxygenase-1 (HO-1) expression. In vivo, echinatin ameliorated LPS-induced lung inflammatory injury, and reduced production of IL-1β and IL-6. These findings demonstrated that echinatin exerted anti-inflammatory effects in vitro and in vivo, via blocking the TAK1-MAPK/NF-κB pathway and activating the Keap1-Nrf2-HO-1 pathway.

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