Eckmaxol Isolated from Ecklonia maxima Attenuates Particulate-Matter-Induced Inflammation in MH-S Lung Macrophage.
D P NagahawattaN M LiyanageH H A C K JayawardhanaThilina U JayawardenaHyo-Geun LeeMoon-Soo HeoYung Hyun ChoiPublished in: Marine drugs (2022)
Airborne particulate matter (PM) originating from industrial processes is a major threat to the environment and health in East Asia. PM can cause asthma, collateral lung tissue damage, oxidative stress, allergic reactions, and inflammation. The present study was conducted to evaluate the protective effect of eckmaxol, a phlorotannin isolated from Ecklonia maxima , against PM-induced inflammation in MH-S macrophage cells. It was found that PM induced inflammation in MH-S lung macrophages, which was inhibited by eckmaxol treatment in a dose-dependent manner (21.0-84.12 µM). Eckmaxol attenuated the expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) in PM-induced lung macrophages. Subsequently, nitric oxide (NO), prostaglandin E-2 (PGE-2), and pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) were downregulated. PM stimulated inflammation in MH-S lung macrophages by activating Toll-like receptors (TLRs), nuclear factor-kappa B (NF-κB), and mitogen-activated protein kinase (MAPK) pathways. Eckmaxol exhibited anti-inflammatory properties by suppressing the activation of TLRs, downstream signaling of NF-κB (p50 and p65), and MAPK pathways, including c-Jun N-terminal kinase (JNK) and p38. These findings suggest that eckmaxol may offer substantial therapeutic potential in the treatment of inflammatory diseases.
Keyphrases
- particulate matter
- oxidative stress
- diabetic rats
- air pollution
- induced apoptosis
- nuclear factor
- nitric oxide synthase
- signaling pathway
- nitric oxide
- high glucose
- ischemia reperfusion injury
- dna damage
- anti inflammatory
- lung function
- toll like receptor
- public health
- poor prognosis
- pi k akt
- drug induced
- heavy metals
- adipose tissue
- healthcare
- endothelial cells
- immune response
- inflammatory response
- long non coding rna
- chronic obstructive pulmonary disease
- hydrogen peroxide
- cell cycle arrest
- cystic fibrosis
- lps induced
- heat shock protein
- polycyclic aromatic hydrocarbons