Format

Send to

Choose Destination
Food Chem Toxicol. 2017 Dec;110:151-155. doi: 10.1016/j.fct.2017.10.027. Epub 2017 Oct 18.

4-Hydroxycinnamic acid protects mice from cigarette smoke-induced pulmonary inflammation via MAPK pathways.

Author information

1
College of Veterinary Medicine BK21 Plus Project Team, Chonnam National University, Gwangju 61186, Republic of Korea.
2
College of Health Sciences, Cheongju University, 298 Daesung-ro, Sangdang-gu, Cheongju-si 360-764, Chungbuk, Republic of Korea.
3
K-herb Research Center, Korea Institute of Oriental Medicine, 1672 Yuseong-daero, Yuseong-gu, Daejeon 34054, Republic of Korea.
4
Research Center, Dongnam Institute of Radiological and Medical Sciences (DIRAMS), Jwadong-gil 40, Gijang-gun, Busan 619-953, Republic of Korea. Electronic address: jskim@dirams.re.kr.
5
College of Veterinary Medicine BK21 Plus Project Team, Chonnam National University, Gwangju 61186, Republic of Korea. Electronic address: dvmmk79@gmail.com.

Abstract

Cigarette smoke (CS) is the main etiological cause of chronic obstructive pulmonary disease, the prevalence of which has continuously increased in recent years. 4-Hydroxycinnamic acid (HA) is a plant phenolic acid that has anti-inflammatory activities. In this study, we explored the therapeutic effects of HA on airway inflammation caused by CS and lipopolysaccharide (LPS) in mice. The animals received 1 h of CS exposure for 7 days and intranasal instillation of LPS on day 4. HA (10 and 20 mg/kg) was administered to animals via oral gavage 1 h before CS exposure. HA treatment significantly decreased the accumulation of inflammatory cells and production of cytokines, including tumor necrosis factor-α, interleukin (IL)-6, and IL-1β, caused by CS and LPS exposure. After histological examination, we observed that HA treatment significantly reduced the infiltration of inflammatory cells into lung tissue caused by CS and LPS exposure. Furthermore, HA-treated groups showed significantly decreased phosphorylation of extracellular signal-regulated kinase, c-Jun N-terminal kinase, p38, and nuclear factor-κB, and activity of cytochrome c oxidase subunit-2 caused by CS and LPS. In conclusion, HA effectively suppresses the airway inflammatory response induced by CS and LPS exposure, and is closely associated with the downregulation of mitogen-activated protein kinases signaling.

KEYWORDS:

4-Hydroxycinnamic acid; Chronic obstructive pulmonary disease; Cigarette smoke; Mitogen-activated protein kinase

PMID:
29054824
DOI:
10.1016/j.fct.2017.10.027
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center