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

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...

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Published inFood 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
LanguageEnglish
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
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Abstract 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.
AbstractList 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.
ABSTRACTTo 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.
Author Hsieh, Wen-Che
Han, Hsin-Hsuan
Lai, Chane-Yu
Tu, Dom-Gene
Chen, Ching-Chung
Chang, Yuan-Yen
Shen, Ting-Jing
Lin, Hui-Wen
Hsieh, Ming-Chang
Lee, Yi-Ju
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  surname: Chang
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Snippet To explore the involved mechanisms and possible treatments of ambient PM2.5 exposure-induced lung inflammation, this work studied the activity of luteolin, a...
ABSTRACTTo explore the involved mechanisms and possible treatments of ambient PM2.5 exposure-induced lung inflammation, this work studied the activity of...
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SubjectTerms 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
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Title Luteolin attenuates PM2.5-induced inflammatory responses by augmenting HO-1 and JAK-STAT expression in murine alveolar macrophages
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