The effect of HMGB1 on sub-toxic chlorpyrifos exposure-induced neuroinflammation in amygdala of neonatal rats. (2nd December 2015)

• Record Type: Journal Article
• Authors: Tian, Jing; Dai, Hongmei; Deng, Yuanying; Zhang, Jie; Li, Ying; Zhou, Jun; Zhao, Mingyi; Zhao, Mengwen; Zhang, Chen; Zhang, Yuxi; Wang, Peipei; Bing, Guoying; Zhao, Lingling
• Is Part Of: Toxicology. Volume 338(2015)
• Page Start: 95
• Page End: 103
• Publication Date: 2015-12-02
• Subjects: CPF chlorpyrifos -- SN substantia nigra -- HMGB1 high-mobility group box 1 -- NF-κB nuclear factor kappa B -- DMSO dimethyl sulfoxide -- IL-6 interleukin-6 -- TNF-α tumor necrosis factor-α; Chlorpyrifos -- Inflammatory -- High-mobility group box 1 -- Nuclear factor kappa B -- Interleukin-6 -- Tumor necrosis factor-α; Toxicology -- Periodicals; Chemicals -- Physiological effect -- Periodicals; 615.9005
• DOI: 10.1016/j.tox.2015.10.010
• Languages: English
• ISSNs: 0300-483X

Abstract

Abstract: Chlorpyrifos (CPF), one of organophosphorus pesticides (OPs), is associated with developmental neurotoxicity. Inflammatory response is closely related with CPF-induced neurotoxicity. The present study aimed at exploring whether sub-toxic CPF exposure on neonatal rats results in neuroinflammation that mediated by HMGB1/TLR4/NF-κB signaling pathway in the amygdala. The neonatal rats were subcutaneously injected with 5 mg/kg CPF for 4 consecutive days (postnatal day 11–14) with or without HMGB1 inhibitor, glycyrrhizin. We assessed the levels of pro-inflammatory cytokines at 12, 24, and 72 h after CPF exposure. The role of HMGB1 on neuroinflammation in sub-toxic exposure during brain development was studied. CPF-treated neonatal rats exhibited a significant increase in the expression of pro-inflammatory cytokines, such as IL-6, TNF-α and HMGB1, and a significant increase in the activation of NF-κB in the amygdala after CPF exposure. Inhibited HMGB1 reduced the release of IL-6 and TNF-α, and inhibited activation of NF-κB. Our findings indicate that CPF exposure on developmental brain might induce the activation of neuroinflammation mediated by HMGB1/TLR4/NF-κB pathway in the amygdala.