Erythropoietin Protects Rat Brain Injury from Carbon Monoxide Poisoning by Inhibiting Toll-Like Receptor 4/NF-kappa B-Dependent Inflammatory Responses.
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.
['Pang|Li|L|', 'Zhang|Nan|N|', 'Dong|Ning|N|', 'Wang|Da-Wei|DW|', 'Xu|Da-Hai|DH|', 'Zhang|Ping|P|', 'Meng|Xiang-Wei|XW|']
D000818:Animals D001930:Brain Injuries D002248:Carbon Monoxide D002249:Carbon Monoxide Poisoning D004487:Edema D004921:Erythropoietin D006624:Hippocampus D007249:Inflammation D053583:Interleukin-1beta D015850:Interleukin-6 D008297:Male D018782:Maze Learning D016328:NF-kappa B D009336:Necrosis D051381:Rats D017207:Rats, Sprague-Dawley D015398:Signal Transduction D051197:Toll-Like Receptor 4 D014409:Tumor Necrosis Factor-alpha
erythropoietin carbon monoxide poisoning toll-like receptor 4 nuclear factor-kappa B inflammatory cytokine