Luteolin attenuates PM2.5-induced inflammatory responses by augmenting HO-1 and JAK-STAT expression in murine alveolar macrophages

• Published in: Food and agricultural immunology Vol. 33; no. 1; pp. 47 - 64
• Main Authors: Hsieh, Wen-Che, Lai, Chane-Yu, Lin, Hui-Wen, Tu, Dom-Gene, Shen, Ting-Jing, Lee, Yi-Ju, Hsieh, Ming-Chang, Chen, Ching-Chung, Han, Hsin-Hsuan, Chang, Yuan-Yen
• Format: Journal Article
• Language: English
• Published: Abingdon Taylor & Francis 31.12.2022; Taylor & Francis Ltd; Taylor & Francis Group
• Subjects: Alveoli; Ambient fine particulate matter (PM2.5); chemokine CCL5; Exposure; Flavonoids; HO-1; Inflammation; Inflammatory response; Interleukin 6; JAK/STAT/NF-κB; Janus kinase 2; lungs; luteolin; Macrophages; mice; Monocyte chemoattractant protein 1; murine alveolar macrophages; NF-κB protein; Nitric-oxide synthase; Particulate matter; Plant species; Pretreatment; Proteins; RANTES; Stat1 protein; Stat3 protein; Tumor necrosis factor-α
• ISSN: 0954-0105; 1465-3443; 1465-3443
• DOI: 10.1080/09540105.2021.2022605

To explore the involved mechanisms and possible treatments of ambient PM2.5 exposure-induced lung inflammation, this work studied the activity of luteolin, a natural flavonoid which widely presents in many plant species, in murine alveolar macrophage MH S cells exposed to PM2.5. Results showed PM2.5 induced an inflammatory response, as evidenced by significantly increased TNF-α, IL-6, MCP-1 and Rantes levels. and induced iNOS, COX-2, and NF-κB protein expressions in MH-S cells. Moreover, luteolin pre-treatment reduced JAK2 and STAT1 but not STAT3 protein expressions in PM2.5-stimulated MH-S cells. Performing JAK2 inhibitor AG490 further showed reduced TNF-α and IL-6 productions as well as iNOS, COX-2, and NF-κB protein expressions. In addition, although PM2.5 exposure could elevate HO-1 expression basically, luteolin pre-treatment and AG490 administration further significantly enhanced HO-1 expression additionally. Collectively, these results revealed that luteolin inhibits inflammation through suppressing JAK2/STAT1/NF-κB pathway and enhancing HO-1 expression in PM2.5-challenged alveolar macrophage MH-S cells.