Oleoylethanolamide Alleviates Hepatic Ischemia-Reperfusion Injury via Inhibiting Endoplasmic Reticulum Stress-Associated Apoptosis.
Oleoylethanolamide Alleviates Hepatic Ischemia-Reperfusion Injury via Inhibiting Endoplasmic Reticulum Stress-Associated Apoptosis.
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油酰乙醇酰胺通过抑制内质网应激相关细胞凋亡减轻肝脏缺血再灌注损伤
DOI：
10.1155/2022/2212996
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发表时间：
2022
期刊：
影响因子：
2.9
通讯作者：
Chen L
中科院分区：
文献类型：
--
作者：
Qi S;Yan Q;Wang Z;Liu D;Zhan M;Du J;Chen L
肝脏缺血/再灌注损伤是肝脏大手术的主要并发症。我们先前的蛋白质组分析研究表明，肝脏缺血/再灌注过程中，过氧化物酶体增殖物激活受体信号级联反应显著上调。为了阐明过氧化物酶体增殖物激活受体α（peroxisome proliferator-activated receptor alpha，PPARα）参与缺血再灌注损伤的可能机制，本研究使用了过氧化物酶体增殖物激活受体α（peroxisome proliferator-activated receptor alpha，PPARα）激动剂油酰乙醇胺（oleoyethanolamide，OEA）。采用小鼠肝部分热缺血再灌注和肝细胞缺氧再给氧模型，证明了OEA对肝I/R损伤的保护作用。其作用机制可能与减轻肝损伤、降低血清ALT和AST水平、减少肝细胞凋亡有关。进一步的机制研究表明，OEA通过激活PPARα调节内质网应激，从而减少内质网应激相关的细胞凋亡，减轻肝I/R损伤。简言之，这些数据首次提出，OEA介导的PPARα激活可能是一种有效的治疗肝脏缺血/再灌注损伤的方法。
Liver ischemia/reperfusion (I/R) injury is a primary complication in major liver surgery. Our previous study about proteome profiling has revealed that the PPAR signaling cascade was significantly upregulated during liver ischemia/reperfusion. To elucidate the potential mechanisms of PPARα involved in I/R injury, we used oleoylethanolamide (OEA), the peroxisome proliferator-activated receptor alpha (PPARα) agonist, in this study. We demonstrated a protective role of OEA on liver I/R injury by using a mouse model of partial warm ischemia-reperfusion and hypoxia-reoxygenation model of hepatocytes. These effects were caused by ameliorating liver damage, decreasing the level of serum ALT and AST, and reducing the apoptosis of hepatocytes. Furthermore, a mechanistic study revealed that OEA regulated endoplasmic reticulum (ER) stress by activating PPARα, thereby reducing ER stress-associated apoptosis to attenuate liver I/R injury. Briefly, these data first proposed that OEA-mediated PPARα activation could be an effective therapy against hepatic ischemia/reperfusion injury.
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影响因子：
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作者：
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DOI：
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