<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>13(3)</volume><submitter>Yang T</submitter><funding>This study was supported by grant from SJTU-STAR Interdisciplinary Research Grant on Medicine and Engineering of Shanghai JiaoTong University</funding><pubmed_abstract>Ischemic stroke is one of the major causes of death and disability among adults. This study sought to explore the mechanism of microRNA (miR)-193b-3p in rats with cerebral ischemia-reperfusion (I/R) injury. The cerebral I/R injury models of rats were established using the suture-occluded method. The pathological changes were observed, and oxidative stress (OS) and mitochondrial function indexes in rat brain tissue were examined. The levels of miR-193b-3p and seven in absentia homolog 1 (SIAH1) were detected. miR-193b-3p agomir or antagomir was injected into the lateral ventricle of I/R rats to overexpress or inhibit miR-193b-3p expression. The targeting relationship between miR-193b-3p and SIAH1 was verified. The effect of SIAH1 overexpression on brain injury in I/R rats was investigated b</pubmed_abstract><journal>Bioengineered</journal><pagination>6942-6954</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8974224</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>MicroRNA-193b-3p reduces oxidative stress and mitochondrial damage in rats with cerebral ischemia-reperfusion injury via the seven in absentia homolog 1/Jun N-terminal kinase pathway.</pubmed_title><pmcid>PMC8974224</pmcid><pubmed_authors>Wu J</pubmed_authors><pubmed_authors>Fan J</pubmed_authors><pubmed_authors>Ge K</pubmed_authors><pubmed_authors>Wang F</pubmed_authors><pubmed_authors>Yang T</pubmed_authors></additional><is_claimable>false</is_claimable><name>MicroRNA-193b-3p reduces oxidative stress and mitochondrial damage in rats with cerebral ischemia-reperfusion injury via the seven in absentia homolog 1/Jun N-terminal kinase pathway.</name><description>Ischemic stroke is one of the major causes of death and disability among adults. This study sought to explore the mechanism of microRNA (miR)-193b-3p in rats with cerebral ischemia-reperfusion (I/R) injury. The cerebral I/R injury models of rats were established using the suture-occluded method. The pathological changes were observed, and oxidative stress (OS) and mitochondrial function indexes in rat brain tissue were examined. The levels of miR-193b-3p and seven in absentia homolog 1 (SIAH1) were detected. miR-193b-3p agomir or antagomir was injected into the lateral ventricle of I/R rats to overexpress or inhibit miR-193b-3p expression. The targeting relationship between miR-193b-3p and SIAH1 was verified. The effect of SIAH1 overexpression on brain injury in I/R rats was investigated b</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Mar</publication><modification>2025-04-19T21:48:47.301Z</modification><creation>2025-04-19T21:48:47.301Z</creation></dates><accession>S-EPMC8974224</accession><cross_references><pubmed>35249453</pubmed><doi>10.1080/21655979.2022.2036398</doi></cross_references></HashMap>