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- Title
Erythropoietin Protects Rat Brain Injury from Carbon Monoxide Poisoning by Inhibiting Toll-Like Receptor 4/NF-kappa B-Dependent Inflammatory Responses.
- Authors
Pang, Li; Zhang, Nan; Dong, Ning; Wang, Da-Wei; Xu, Da-Hai; Zhang, Ping; Meng, Xiang-Wei
- 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.
- Subjects
ERYTHROPOIETIN; PHYSIOLOGICAL effects of carbon monoxide; BRAIN injuries; TOLL-like receptors; NF-kappa B; CYTOKINES; INFLAMMATION; THERAPEUTICS
- Publication
Inflammation, 2016, Vol 39, Issue 2, p561
- ISSN
0360-3997
- Publication type
Article
- DOI
10.1007/s10753-015-0280-4