Duchesnea indica Extract Attenuates Coal Fly Ash-Induced Inflammation in Murine Alveolar Macrophages through the NF-Kappa B Pathway

• Published in: Evidence-based complementary and alternative medicine Vol. 2021; pp. 1 - 11
• Main Authors: Ullah, H. M. Arif, Lee, Yuan Yee, Kim, Sung Dae, Rhee, Man Hee
• Format: Journal Article
• Language: English
• Published: New York Hindawi 2021; Hindawi Limited
• Subjects: Acids; Alternative medicine; Alveoli; Anti-inflammatory agents; Cell culture; Cell cycle; Cell viability; Chromatography; Coal; Cyclooxygenase-2; Cytokines; Cytotoxicity; Duchesnea indica; Fly ash; Gas chromatography; Gene expression; IL-1β; Immune system; Immunofluorescence; Inflammation; Interleukin 6; Liquid chromatography; Lungs; Macrophages; Mass spectroscopy; Nanoparticles; NF-κB protein; Nitric oxide; Nitric-oxide synthase; Outdoor air quality; Polymerase chain reaction; Reagents; Signal transduction; Tumor necrosis factor-α; Western blotting; St Louis Missouri; United States > US; South Korea
• ISSN: 1741-427X; 1741-4288
• DOI: 10.1155/2021/5546052

Duchesnea indica is known as false strawberry, is found in East Asia, and has numerous biological properties. The aim of this study was to investigate the anti-inflammatory effect of Duchesnea indica extract (DIE) on coal fly ash- (CFA-) induced inflammation in murine alveolar macrophages (MH-S). Following the induction of inflammation in MH-S cells by CFA, nitric oxide (NO) was measured to evaluate the anti-inflammatory property of DIE. Cell viability and inflammatory gene expression were analyzed using polymerase chain reaction (PCR). The inflammatory pathway in MH-S cells was determined via western blotting and immunofluorescence (IF) analysis. Finally, the major components of the DIE were identified and separated through ultra-performance liquid chromatography (UPLC) and gas chromatography-mass spectrometry (GC-MS) analysis. Our results showed that the DIE dose-dependently inhibited the CFA-induced NO production in MH-S cells. Moreover, the DIE could suppress the CFA-induced proinflammatory mediators, such as cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS). In addition, the inhibitory effect of the DIE on proinflammatory cytokines, including interleukin-6 (IL-6), IL-1β, and tumor necrosis factor-α (TNF-α), was detected with PCR. Moreover, the effect of the DIE on the nuclear factor-κB (NF-κB) pathway in CFA-activated MH-S cells was measured via western blotting. Furthermore, the inhibition of the phosphorylated NF-κB (p-NF-κB) translocation was analyzed using IF assay. The findings of this study indicated that the DIE potentially inhibited the CFA-induced inflammation by blocking the NF-κB inflammatory signaling pathway in MH-S cells and that the DIE might contain favorable anti-inflammatory compounds which may be effective in attenuating lung inflammation.