<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lin J</submitter><funding>Key Research and Development Program of Zhejiang</funding><funding>Natural Science Foundation of Zhejiang Province</funding><funding>Research Funds project of Wenzhou Medical University</funding><funding>National Natural Science Foundation of China</funding><funding>Zhejiang Provincial Science and Technology Innovation Program (New Young Talent Program) for College Students</funding><pagination>2133</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9690185</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(11)</volume><pubmed_abstract>Pyroptosis serves a crucial function in various types of ischemia and reperfusion injuries. Oridonin, a tetracycline diterpene derived from &lt;i>Rabdosia rubescens&lt;/i>, can significantly inhibit the aggregation of NLRP3-mediated inflammasome. This experiment is aimed at investigating the effect of oridonin on pyroptosis in mice cardiomyocytes. Based on the models of myocardial ischemia/reperfusion (I/R) and hypoxia/reoxygenation (H/R), Evans Blue/TTC double staining, TUNEL staining, and Western blotting were applied to determine the effects of oridonin on myocardial damage, cellular activity and signaling pathways involved in pyroptosis. During I/R and H/R treatments, the extent of gasdermin D-N domains was upregulated in cardiomyocytes. Apart from that, oridonin improved cell survival in vi</pubmed_abstract><journal>Genes</journal><pubmed_title>Oridonin Protects against Myocardial Ischemia-Reperfusion Injury by Inhibiting GSDMD-Mediated Pyroptosis.</pubmed_title><pmcid>PMC9690185</pmcid><funding_grant_id>2021R413010</funding_grant_id><funding_grant_id>LQ21H020009</funding_grant_id><funding_grant_id>82003750</funding_grant_id><funding_grant_id>82070446</funding_grant_id><funding_grant_id>2019C03012</funding_grant_id><funding_grant_id>KYYW202017</funding_grant_id><pubmed_authors>Lai X</pubmed_authors><pubmed_authors>Fan X</pubmed_authors><pubmed_authors>Shi S</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Huang W</pubmed_authors><pubmed_authors>Ye B</pubmed_authors><pubmed_authors>Su L</pubmed_authors><pubmed_authors>Lin J</pubmed_authors><pubmed_authors>Shao R</pubmed_authors><pubmed_authors>Ying M</pubmed_authors><pubmed_authors>Zhong L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Oridonin Protects against Myocardial Ischemia-Reperfusion Injury by Inhibiting GSDMD-Mediated Pyroptosis.</name><description>Pyroptosis serves a crucial function in various types of ischemia and reperfusion injuries. Oridonin, a tetracycline diterpene derived from &lt;i>Rabdosia rubescens&lt;/i>, can significantly inhibit the aggregation of NLRP3-mediated inflammasome. This experiment is aimed at investigating the effect of oridonin on pyroptosis in mice cardiomyocytes. Based on the models of myocardial ischemia/reperfusion (I/R) and hypoxia/reoxygenation (H/R), Evans Blue/TTC double staining, TUNEL staining, and Western blotting were applied to determine the effects of oridonin on myocardial damage, cellular activity and signaling pathways involved in pyroptosis. During I/R and H/R treatments, the extent of gasdermin D-N domains was upregulated in cardiomyocytes. Apart from that, oridonin improved cell survival in vi</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Nov</publication><modification>2025-04-19T14:44:17.307Z</modification><creation>2025-04-19T14:44:17.307Z</creation></dates><accession>S-EPMC9690185</accession><cross_references><pubmed>36421808</pubmed><doi>10.3390/genes13112133</doi></cross_references></HashMap>