Anti-Inflammatory Effects of Phlebia sp. Extract in Lipopolysaccharide-Stimulated RAW 264.7 Macrophages

• Published in: BioMed research international Vol. 2022; pp. 1 - 10
• Main Authors: Lim, Eui Hyeon, Mun, Seul-Ki, Kim, Jong-Jin, Chang, Dong-Jo, Yee, Sung-Tae
• Format: Journal Article
• Language: English
• Published: New York Hindawi 14.07.2022; Hindawi Limited
• Subjects: Activator protein 1; Algae; Anti-inflammatory agents; Antibodies; Biomedical research; c-Fos protein; c-Jun protein; Chemokines; Colony-stimulating factor; Cytokines; Cytotoxicity; Granulocyte-macrophage colony stimulating factor; IL-1β; Inflammation; Interleukin 6; Kinases; Laboratories; Lipopolysaccharides; Macrophages; MAP kinase; NF-κB protein; Nitric oxide; Pathogens; Phosphorylation; Prostaglandin E2; Protein kinase; Proteins; Ribosomal DNA; Signaling; Transcription factors; Tumor necrosis factor-α; Variance analysis; United States > US; Japan
• ISSN: 2314-6133; 2314-6141
• DOI: 10.1155/2022/2717196

Lichens are a life form in which algae and fungi have a symbiotic relationship and have various biological activities, including anti-inflammatory and antiproliferative activities. This is the first study to investigate the anti-inflammatory activity of a Phlebia sp. fungal extract (PSE) isolated from Peltigera neopolydactyla in lipopolysaccharide- (LPS-) stimulated RAW 264.7 macrophage. PSE reduced the production of the proinflammatory cytokine (tumor necrosis factor-α, interleukin-6, and interleukin-1β), chemokine (granulocyte-macrophage colony-stimulating factor), nitric oxide, and prostaglandin E2 in the LPS-stimulated RAW264.7 macrophages. Especially, PSE inhibits the phosphorylation of activator protein-1 (AP-1) signaling (c-Fos and c-Jun) and their upstream mitogen-activated protein kinase kinases/mitogen-activated protein kinases (MKK/MAPKs: MKK4, MKK7, and JNK) and finally reduced the production of the inflammatory cytokines. The inhibitory effects mainly act via suppressing JNK-mediated AP-1 rather than the NF-κB pathway. Furthermore, PSE inhibited the production of final inflammatory effector molecules involved in AP-1 signaling, including nitric oxide (NO) and prostaglandin E2 (PGE2). Here, we report that PSE has the potential to be developed as an anti-inflammatory agent.