TY  - JOUR
PY  - 2015//
TI  - Erythropoietin protects rat brain injury from carbon monoxide poisoning by inhibiting toll-like receptor 4/NF-kappa B-dependent inflammatory responses
JO  - Inflammation
A1  - Pang, Li
A1  - Zhang, Nan
A1  - Dong, Ning
A1  - Wang, Da-Wei
A1  - Xu, Da-Hai
A1  - Zhang, Ping
A1  - Meng, Xiang-Wei
SP  - 561
EP  - 568
VL  - 39
IS  - 2
N2  - 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.<p />  <p>Language: en</p>
LA  - en
SN  - 0360-3997
UR  - http://dx.doi.org/10.1007/s10753-015-0280-4
ID  - ref1
ER  -