Citation

Pang L, Zhang N, Dong N, Wang DW, Xu DH, Zhang P, Meng XW. Inflammation 2015; 39(2): 561-568.

Affiliation

Department of Gastrointestinal Medicine, The First Hospital of Jilin University, 71 Xinmin Road, Changchun, 130021, China. xiangweimeng2003@163.com.

Copyright

(Copyright © 2015, Holtzbrinck Springer Nature Publishing Group)

DOI

10.1007/s10753-015-0280-4

PMID

26521252

Abstract

Inflammatory responses play critical roles in carbon monoxide (CO) poisoning-induced cerebral injury. The present study investigated whether erythropoietin (EPO) modulates the toll-like receptor 4 (TLR4) and nuclear factor-kappa B (NF-κB) inflammatory signaling pathways in brain injury after acute CO poisoning. EPO (2500 and 5000 U/kg) was injected subcutaneously twice a day after acute CO poisoning for 2 days. At 48 h after treatment, the expression levels of TLR4 and NF-κB as well as the levels of inflammatory cytokines in the hippocampal tissues were measured. Our results showed that CO poisoning induced a significant upregulation of TLR4, NF-κB, and inflammatory cytokines in the injured rat hippocampal tissues. Treatment with EPO remarkably suppressed the gene and protein expression levels of TLR4 and NF-κB, as well as the concentrations of TNF-α, IL-1β, and IL-6 in the hippocampal tissues. EPO treatment ameliorated CO poisoning-induced histological edema and neuronal necrosis. These results suggested that EPO protected against CO poisoning-induced brain damage by inhibiting the TLR4-NF-κB inflammatory signaling pathway.

Language: en