Isoleucilactucin Ameliorates Coal Fly Ash-Induced Inflammation through the NF-κB and MAPK Pathways in MH-S Cells

• Published in: International journal of molecular sciences Vol. 22; no. 17; p. 9506
• Main Authors: Ullah, H. M. Arif, Kwon, Tae-Hyung, Park, SeonJu, Kim, Sung Dae, Rhee, Man Hee
• Format: Journal Article
• Language: English
• Published: Basel MDPI AG 01.09.2021; MDPI
• Subjects: Alveoli; AMPK pathway; Anti-inflammatory agents; anti-inflammatory properties; Asthma; Chronic illnesses; Chronic obstructive pulmonary disease; Coal; Cyclooxygenase-2; Cytokines; Fly ash; Gene expression; Inflammation; Inflammatory diseases; Interleukin 6; Investigations; isoleucilactucin; Kinases; lung macrophages; Macrophages; MAP kinase; NF-κB pathway; NF-κB protein; Nitric oxide; Nitric-oxide synthase; Nuclear transport; Phosphorylation; Pollutants; Protein kinase; Tumor necrosis factor-TNF; Tumor necrosis factor-α; South Korea
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms22179506

We investigated whether isoleucilactucin, an active constituent of Ixeridium dentatum, reduces inflammation caused by coal fly ash (CFA) in alveolar macrophages (MH-S). The anti-inflammatory effects of isoleucilactucin were assessed by measuring the concentration of nitric oxide (NO) and the expression of pro-inflammatory mediators in MH-S cells exposed to CFA-induced inflammation. We found that isoleucilactucin reduced CFA-induced NO generation dose-dependently in MH-S cells. Moreover, isoleucilactucin suppressed CFA-activated proinflammatory mediators, including cyclooxygenase-2 (COX2) and inducible NO synthase (iNOS), and the proinflammatory cytokines such as interleukin-(IL)-1β, IL-6, and tumor necrosis factor (TNF-α). The inhibiting properties of isoleucilactucin on the nuclear translocation of phosphorylated nuclear factor-kappa B (p-NF-κB) were observed. The effects of isoleucilactucin on the NF-κB and mitogen-activated protein kinase (MAPK) pathways were also measured in CFA-stimulated MH-S cells. These results indicate that isoleucilactucin suppressed CFA-stimulated inflammation in MH-S cells by inhibiting the NF-κB and MAPK pathways, which suggest it might exert anti-inflammatory properties in the lung.