ALCAM Deficiency Alleviates LPS-Induced Acute Lung Injury by Inhibiting Inflammatory Response

Li, Ruirui; Ren, Tao; Zeng, Jianqiong; Xu, Hang

doi:10.1007/s10753-022-01765-3

Cited by 5 publications

(2 citation statements)

References 44 publications

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“…Furthermore, the results of pathological examination demonstrated that both echinatin and DEX could significantly reduce the increase of LPS-induced lung injury scores in mice ( Fig 8B ). Furthermore, several of the cytokines are also involved in the progression of ALI, including IL-1β and IL-6 [ 3 ]. Consistent with the histological examination staining results, tail intravenous LPS injection markedly increased the serum levels of IL-1β and IL-6, and echinatin or DEX could reverse the production of these pro-inflammatory cytokines ( Fig 8C and 8D ).…”

Section: Resultsmentioning

confidence: 99%

“…Acute lung injury (ALI) is a chronic clinical syndrome caused by serious inflammatory damage that could progress to life-threatening acute respiratory distress syndrome (ARDS) unless promptly treated [ 1 , 2 ]. The pathology of ALI is characterized by the activation and infiltration of inflammatory cells, respiratory distress, and diffuse pulmonary edema [ 3 , 4 ]. ALI is generally caused by various internal and external factors including sepsis, pneumonia, ischemia reperfusion, drug toxicity, and trauma [ 1 , 5 ].…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Resultsmentioning

confidence: 99%