<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>2022</volume><submitter>Qi S</submitter><pubmed_abstract>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 PPAR&lt;i>α&lt;/i> involved in I/R injury, we used oleoylethanolamide (OEA), the peroxisome proliferator-activated receptor alpha (PPAR&lt;i>α&lt;/i>) 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</pubmed_abstract><journal>PPAR research</journal><pagination>2212996</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8960015</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Oleoylethanolamide Alleviates Hepatic Ischemia-Reperfusion Injury via Inhibiting Endoplasmic Reticulum Stress-Associated Apoptosis.</pubmed_title><pmcid>PMC8960015</pmcid><pubmed_authors>Zhan M</pubmed_authors><pubmed_authors>Yan Q</pubmed_authors><pubmed_authors>Chen L</pubmed_authors><pubmed_authors>Du J</pubmed_authors><pubmed_authors>Liu D</pubmed_authors><pubmed_authors>Qi S</pubmed_authors><pubmed_authors>Wang Z</pubmed_authors></additional><is_claimable>false</is_claimable><name>Oleoylethanolamide Alleviates Hepatic Ischemia-Reperfusion Injury via Inhibiting Endoplasmic Reticulum Stress-Associated Apoptosis.</name><description>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 PPAR&lt;i>α&lt;/i> involved in I/R injury, we used oleoylethanolamide (OEA), the peroxisome proliferator-activated receptor alpha (PPAR&lt;i>α&lt;/i>) 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</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2025-04-19T20:13:07.549Z</modification><creation>2025-04-19T20:13:07.549Z</creation></dates><accession>S-EPMC8960015</accession><cross_references><pubmed>35356086</pubmed><doi>10.1155/2022/2212996</doi></cross_references></HashMap>