Format

Send to

Choose Destination
Environ Toxicol. 2019 Apr;34(4):486-494. doi: 10.1002/tox.22702. Epub 2019 Jan 4.

Expression of pro-inflammatory cytokines and mediators induced by Bisphenol A via ERK-NFκB and JAK1/2-STAT3 pathways in macrophages.

Author information

1
Department of Dentistry, Chung Shan Medical University Hospital, Taichung, Taiwan.
2
School of Dentistry, Chung Shan Medical University, Taichung, Taiwan.
3
School of Public Health, Chung Shan Medical University, Taichung, Taiwan.
4
Department of Anatomy, School of Medicine, Chung Shan Medical University, Taichung, Taiwan.
5
Department of Pharmacology, School of Medicine, Chung Shan Medical University, Taichung, Taiwan.
6
Department of Pharmacy, Chung Shan Medical University Hospital, Taichung, Taiwan.

Abstract

Macrophages not only play an important role in the innate immune response but also participate in many inflammatory and infectious diseases including asthma, diabetes, obesity, cardiovascular diseases, and cancers. Bisphenol A (BPA) is the most commonly used component for plastic products. However, BPA is an endocrine disruptor for mammals and participates in several inflammatory and infectious diseases. Up until now, there are no researches demonstrated the potential role of BPA in macrophage activation and its relative mechanism. BPA promoted the generation of proinflammatory cytokines IL-1β, IL-6, and TNFα in a concentration-dependent manner (P < 0.05). BPA was identified to increase the expression of proinflammatory mediators NO and PGE2, and its upstream factors iNOS, COX2, and cPLA2 in a concentration-dependent manner (P < 0.05). Phosphorylation and nuclear translocation of NF-κB p65 were significantly induced by BPA via IκB degradation (P < 0.05). In addition, phosphorylation of ERK significantly induced by BPA at a concentration which was less than that for phosphorylation of p38 MAPK and JNK (P < 0.05). Furthermore, phosphorylation of STAT3 significantly induced by BPA at a concentration lower than that for phosphorylation of STAT1 (P < 0.05). Phosphorylation of JAK1 and JAK2 was also significantly induced by BPA in a concentration-dependent manner (P < 0.05).

KEYWORDS:

ERK-NFκB; JAK1/2-STAT3; bisphenol A; macrophages; proinflammatory mediators

PMID:
30609183
DOI:
10.1002/tox.22702
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Wiley
Loading ...
Support Center