TY - JOUR
T1 - The effect of HMGB1 on sub-toxic chlorpyrifos exposure-induced neuroinflammation in amygdala of neonatal rats
AU - Tian, Jing
AU - Dai, Hongmei
AU - Deng, Yuanying
AU - Zhang, Jie
AU - Li, Ying
AU - Zhou, Jun
AU - Zhao, Mingyi
AU - Zhao, Mengwen
AU - Zhang, Chen
AU - Zhang, Yuxi
AU - Wang, Peipei
AU - Bing, Guoying
AU - Zhao, Lingling
N1 - Publisher Copyright:
© 2015 Z.
PY - 2015/12/2
Y1 - 2015/12/2
N2 - 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.
AB - 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.
KW - Chlorpyrifos
KW - High-mobility group box 1
KW - Inflammatory
KW - Interleukin-6
KW - Nuclear factor kappa B
KW - Tumor necrosis factor-α
UR - http://www.scopus.com/inward/record.url?scp=84946576373&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84946576373&partnerID=8YFLogxK
U2 - 10.1016/j.tox.2015.10.010
DO - 10.1016/j.tox.2015.10.010
M3 - Article
C2 - 26524701
AN - SCOPUS:84946576373
SN - 0300-483X
VL - 338
SP - 95
EP - 103
JO - Toxicology
JF - Toxicology
ER -