首页> 外文会议>International Conference on Frontiers of Biological Sciences and Engineering >Protective Role of N-Acetyl-L-Tryptophan against Hepatic Ischemia-Reperfusion Injury by the TLR4/NF-KB Signaling pathway
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Protective Role of N-Acetyl-L-Tryptophan against Hepatic Ischemia-Reperfusion Injury by the TLR4/NF-KB Signaling pathway

机译:N-乙酰-1-色氨酸对TLR4 / NF-KB信号通路对肝缺血再灌注损伤的保护作用

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Background: Hepatic Ischemia-reperfusion injury (HIRI) is a complex process during liver resection and transplantation.The purpose of this study was to investigate whether N-acetyl-L-tryptophan (L-NAT) could protect hepatocytes against acute hepatic ischemia-reperfusion injury through the Toll-Like Receptor 4(TLR4)/nuclear transcription factor-KB (NF-kB) signaling pathway and its possible mechanisms. Methods: The expression of SP and NK-1R were detected in rat models of hepatic ischemia-reperfusion injury .The activity of NF-kB and TLR4 were detected in H202-induced by the BRL oxidative damage model. Results: (1) Immunohistochemical staining showed that the expression of substanceP (SP) and Neuroknin 1 Receptor (NK-1R) increased after hepatic ischemia-reperfusion injury (HIRI). (2)L-NAT pretreatment could inhibit the expression of nuclear transcription factor Kappa-B (NF-kB) and toll-like receptor 4 (TLR4) induced by HIRI. Conclusion: Taken together, the increased of SP and NK- 1R after HIRI revealing that neurogenic inflammatory responsewas involved inHIRI. The results that L-NATsignificantly decreased the increasing of NF-kB and TLR4induced byHIRI implies that L-NAT protects liver against hepatic ischemia-reperfusion injury through TLR4/NF-kB signaling pathway.
机译:背景:肝脏缺血再灌注损伤(HIRI)是肝切除和这项研究的目的transplantation.The在一个复杂的过程是调查N-乙酰基L-色氨酸(L-NAT)是否能保护肝细胞对急性肝缺血再灌注通过Toll样受体4(TLR4)/核转录因子κB(NF-KB)信号传导途径和其可能的作用机制的伤害。方法:在大鼠模型NF-kB和TLR4的肝缺血 - 再灌注损伤.The活性的检测SP和NK-1R的表达在H 2 O 2诱导的由BRL氧化损伤模型进行检测。结果:(1)免疫组织化学染色表明,P物质(SP)和Neuroknin 1受体(NK-1R)的表达肝缺血 - 再灌注损伤(HIRI)后增加。 (2)L-NAT预处理能抑制核转录因子κB-B(NF-KB)的由HIRI诱导表达和toll样受体4(TLR4)。结论:总之,HIRI揭示神经源性炎症responsewas涉及inHIRI后增加的SP和NK-1R的。的结果表明,L-NATsignificantly降低NF-κB的增加和TLR4induced byHIRI意味着L-NAT通过TLR4 / NF-kB信号传导途径防止肝脏缺血 - 再灌注损伤肝脏。

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