4.7 Article

Nonylphenol attenuates SOCS3 expression and M1 polarization in lipopolysaccharide-treated rat splenic macrophages

期刊

ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
卷 174, 期 -, 页码 574-583

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ecoenv.2019.03.012

关键词

Endocrine disruption; Inflammation; NF-kappa 3; Cytokines; SOCS3; Nonylphenol

资金

  1. Department of Science and Technology, Government of India [SR/FST/LSII 031/2013(c)]
  2. University Grants Commission, Government of India [F.5-11/2012 [SAP-II]]

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Endocrine disruptors interfere with normal sexual and reproductive development of numerous organisms. Widely used in several chemical and manufacturing industries, nonylphenol (NP), a potent xenoestrogen, has the potential to perturb immune system. Using rat splenic macrophages (SM Phi) as the model system, NP-modulation of lipopolysaccharide (LPS)-induced inflammatory response has been investigated. Our results demonstrate that NP (0.1-10 mu M) attenuates catalase activity, reactive oxygen species (ROS) generation and nitric oxide (NO) synthesis in LPS-treated SM Phi in vitro. NP inhibition of LPS-induced nuclear factor kappa B (NF-kappa B) activation and pro inflammatory cytokine gene expression corroborate well with attenuation of suppressor of cytokine signalling 3 (SOCS3). Besides, elevated expression of anti-inflammatory factors reveals inverse correlation with suppression of endotoxin-induced Ml polarization in NP pre-incubated cells. While LPS promotes, NP prevents ERK1/2 (extra cellular-signal-regulated kinase 1/2) phosphorylation and MEK-inhibitor abrogates SOCS3 expression and NO production suggesting involvement of ERK1/2 in NP inhibition of SOCS3 expression. Further, translational inhibitor cycloheximide prevents LPS-induced NF-kappa B activation indicating functional importance of de novo synthesis of SOCS3, at least in part, in toll-like receptor 4 (TLR4)-mediated inflammatory response. Collectively, present study provides evidence favouring participation of SOCS3 in NP modulation of inflammatory response in rat SM Phi.

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