Methyl P-Coumarate Ameliorates the Inflammatory Response in Activated-Airway Epithelial Cells and Mice with Allergic Asthma.
Ji-Won ParkJinseon ChoiJuhyun LeeJin-Mi ParkSeong-Man KimJae-Hong MinDa-Yun SeoSoo-Hyeon GooJu-Hee KimOk-Kyoung KwonKihoon LeeKyung-Seop AhnSei-Ryang OhJae-Won LeePublished in: International journal of molecular sciences (2022)
Methyl p-coumarate (methyl p-hydroxycinnamate) (MH) is a natural compound found in a variety of plants. In the present study, we evaluated the ameliorative effects of MH on airway inflammation in an experimental model of allergic asthma (AA). In this in vitro study, MH was found to exert anti-inflammatory activity on PMA-stimulated A549 airway epithelial cells by suppressing the secretion of IL-6, IL-8, MCP-1, and ICAM-1. In addition, MH exerted an inhibitory effect not only on NF-κB (p-NF-κB and p-IκB) and AP-1 (p-c-Fos and p-c-Jun) activation but also on A549 cell and EOL-1 cell (eosinophil cell lines) adhesion. In LPS-stimulated RAW264.7 macrophages, MH had an inhibitory effect on TNF-α, IL-1β, IL-6, and MCP-1. The results from in vivo study revealed that the increases in eosinophils/Th2 cytokines/MCP-1 in the bronchoalveolar lavage fluid (BALF) and IgE in the serum of OVA-induced mice with AA were effectively inhibited by MH administration. MH also exerted a reductive effect on the immune cell influx, mucus secretion, and iNOS/COX-2 expression in the lungs of mice with AA. The effects of MH were accompanied by the inactivation of NF-κB. Collectively, the findings of the present study indicated that MH attenuates airway inflammation in mice with AA, suggesting its potential as an adjuvant in asthma therapy.
Keyphrases
- signaling pathway
- single cell
- oxidative stress
- chronic obstructive pulmonary disease
- rheumatoid arthritis
- lung function
- immune response
- metabolic syndrome
- transcription factor
- mesenchymal stem cells
- stem cells
- nuclear factor
- nitric oxide
- skeletal muscle
- air pollution
- endothelial cells
- staphylococcus aureus
- toll like receptor
- insulin resistance
- mouse model
- nitric oxide synthase
- smoking cessation
- lipopolysaccharide induced
- drug induced
- candida albicans
- diabetic rats