<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Che Y</submitter><funding>Natural Science Foundation of Jiangxi Province</funding><pagination>6839-6855</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8973660</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>13(3)</volume><pubmed_abstract>microRNAs, as small endogenous RNAs, influence umpteen sophisticated cellular biological functions regarding neurodegenerative and cerebrovascular diseases. Here, we interrogated miR-381-3p's influence on BV2 activation and neurotoxicity in ischemic and hypoxic environment. Oxygen-glucose deprivation (OGD) was adopted to induce microglial activation and HT-22 neuron damage. Quantitative polymerase chain reaction (qRT-PCR) was taken to check miR-381-3p expression in OGD-elicited BV2 cells and HT-22 neurons. It transpired that miR-381-3p expression was lowered in BV2 cells and HT-22 cells elicited by OGD. miR-381-3p up-regulation remarkably hampered inflammatory mediator expression in BV2 cells induced by OGD and weakened HT22 neuron apoptosis. &lt;i>In vivo&lt;/i>, miR-381-3p expression was abate</pubmed_abstract><journal>Bioengineered</journal><pubmed_title>Overexpression of microRNA-381-3p ameliorates hypoxia/ischemia-induced neuronal damage and microglial inflammation via regulating the C-C chemokine receptor type 2 /nuclear transcription factor-kappa B axis.</pubmed_title><pmcid>PMC8973660</pmcid><funding_grant_id>20202BAB206061</funding_grant_id><pubmed_authors>Li X</pubmed_authors><pubmed_authors>He J</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Che Y</pubmed_authors><pubmed_authors>Wu D</pubmed_authors><pubmed_authors>Yuan G</pubmed_authors></additional><is_claimable>false</is_claimable><name>Overexpression of microRNA-381-3p ameliorates hypoxia/ischemia-induced neuronal damage and microglial inflammation via regulating the C-C chemokine receptor type 2 /nuclear transcription factor-kappa B axis.</name><description>microRNAs, as small endogenous RNAs, influence umpteen sophisticated cellular biological functions regarding neurodegenerative and cerebrovascular diseases. Here, we interrogated miR-381-3p's influence on BV2 activation and neurotoxicity in ischemic and hypoxic environment. Oxygen-glucose deprivation (OGD) was adopted to induce microglial activation and HT-22 neuron damage. Quantitative polymerase chain reaction (qRT-PCR) was taken to check miR-381-3p expression in OGD-elicited BV2 cells and HT-22 neurons. It transpired that miR-381-3p expression was lowered in BV2 cells and HT-22 cells elicited by OGD. miR-381-3p up-regulation remarkably hampered inflammatory mediator expression in BV2 cells induced by OGD and weakened HT22 neuron apoptosis. &lt;i>In vivo&lt;/i>, miR-381-3p expression was abate</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Mar</publication><modification>2026-03-18T14:18:35.852Z</modification><creation>2025-08-23T03:08:57.528Z</creation></dates><accession>S-EPMC8973660</accession><cross_references><pubmed>35246016</pubmed><doi>10.1080/21655979.2022.2038448</doi></cross_references></HashMap>