Erythropoietin Protects Rat Brain Injury from Carbon Monoxide Poisoning by Inhibiting Toll-Like Receptor 4/NF-kappa B-Dependent Inflammatory Responses
Erythropoietin Protects Rat Brain Injury from Carbon Monoxide Poisoning by Inhibiting Toll-Like Receptor 4/NF-kappa B-Dependent Inflammatory Responses
复制标题
促红细胞生成素通过抑制 Toll 样受体 4/NF-kappa B 依赖性炎症反应，保护大鼠脑损伤免遭一氧化碳中毒。
DOI：
10.1007/s10753-015-0280-4
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发表时间：
2016-04-01
期刊：
影响因子：
5.1
通讯作者：
Meng, Xiang-Wei
中科院分区：
文献类型：
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作者：
Pang, Li;Zhang, Nan;Meng, Xiang-Wei
炎症反应在一氧化碳（CO）中毒引起的脑损伤中起关键作用。本研究旨在探讨促红细胞生成素（EPO）是否调节急性CO中毒后脑损伤中Toll样受体4（TLR 4）和核因子-κ B（NF-κ B）炎症信号通路。急性CO中毒后，连续2天皮下注射EPO（2500和5000 U/kg），每日2次。治疗后48 h，检测海马组织TLR 4、NF-κ B的表达水平以及炎症细胞因子的水平。我们的研究结果表明，CO中毒诱导TLR 4，NF-κ B B，和炎症细胞因子在损伤的大鼠海马组织中的显着上调。EPO治疗显著抑制了海马组织中TLR 4和NF-κ B B的基因和蛋白表达水平，以及TNF-α、IL-1 β和IL-6的浓度。EPO治疗改善了CO中毒引起的组织水肿和神经元坏死。这些结果表明，EPO通过抑制TLR 4-NF-κ B炎症信号通路保护CO中毒诱导的脑损伤。
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-kappa B) 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-kappa B 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-kappa B, and inflammatory cytokines in the injured rat hippocampal tissues. Treatment with EPO remarkably suppressed the gene and protein expression levels of TLR4 and NF-kappa B, as well as the concentrations of TNF-alpha, IL-1 beta, 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-kappa B inflammatory signaling pathway.