<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>13</volume><submitter>Li S</submitter><funding>Key Technologies Research and Development Program</funding><funding>Natural Science Foundation of Shandong Province</funding><funding>National Natural Science Foundation of China</funding><pubmed_abstract>The molecular mechanism underlying the protective role of propofol against myocardial ischemia/reperfusion (I/R) injury remains poorly understood. Previous studies have shown that ferroptosis is an imperative pathological process in myocardial I/R injury. We hypothesized that propofol prevents myocardial I/R injury by inhibiting ferroptosis via the AKT/p53 signaling pathway. The ferroptosis-inducing agent erastin (E) and AKT inhibitor MK2206 (MK) were used to investigate the role of propofol in myocardial I/R injury. H9C2 cells treated without any reagents, erastin for 24 h, propofol for 1 h before adding erastin were assigned as the control (C), E, and E + P group, respectively. Cell viability, reactive oxygen species (ROS), and the expression of antioxidant enzymes, including ferritin he</pubmed_abstract><journal>Frontiers in pharmacology</journal><pagination>841410</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8966655</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Propofol Protects Myocardium From Ischemia/Reperfusion Injury by Inhibiting Ferroptosis Through the AKT/p53 Signaling Pathway.</pubmed_title><pmcid>PMC8966655</pmcid><pubmed_authors>Yang X</pubmed_authors><pubmed_authors>Zhao M</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Li S</pubmed_authors><pubmed_authors>Lei Z</pubmed_authors><pubmed_authors>Wang D</pubmed_authors><pubmed_authors>Tang S</pubmed_authors><pubmed_authors>Yu J</pubmed_authors><pubmed_authors>Hou Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>Propofol Protects Myocardium From Ischemia/Reperfusion Injury by Inhibiting Ferroptosis Through the AKT/p53 Signaling Pathway.</name><description>The molecular mechanism underlying the protective role of propofol against myocardial ischemia/reperfusion (I/R) injury remains poorly understood. Previous studies have shown that ferroptosis is an imperative pathological process in myocardial I/R injury. We hypothesized that propofol prevents myocardial I/R injury by inhibiting ferroptosis via the AKT/p53 signaling pathway. The ferroptosis-inducing agent erastin (E) and AKT inhibitor MK2206 (MK) were used to investigate the role of propofol in myocardial I/R injury. H9C2 cells treated without any reagents, erastin for 24 h, propofol for 1 h before adding erastin were assigned as the control (C), E, and E + P group, respectively. Cell viability, reactive oxygen species (ROS), and the expression of antioxidant enzymes, including ferritin he</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2025-04-05T00:27:47.619Z</modification><creation>2025-02-19T00:29:24.354Z</creation></dates><accession>S-EPMC8966655</accession><cross_references><pubmed>35370724</pubmed><doi>10.3389/fphar.2022.841410</doi></cross_references></HashMap>