{"title":"MiRNA-384-5p靶向GABRB1调节氯胺酮诱导的神经元神经毒性。","authors":"Qiange Yang, Feiyu Long","doi":"10.5137/1019-5149.JTN.36367-21.2","DOIUrl":null,"url":null,"abstract":"<p><strong>Aim: </strong>To determine the function of miR-384-5p in ketamine-induced neurotoxicity.</p><p><strong>Material and methods: </strong>Neonatal hippocampal neurons were isolated from rats and treated with varying doses of ketamine. RT-qPCR was utilized to measure the miR-384-5p level in ketamine-treated neurons. Neuronal viability was evaluated by MTT assay. TUNEL staining and flow cytometry were applied to measure neuronal apoptosis. H2-DCFDA staining was utilized to detect the intracellular ROS level. Protein levels were measured using Western blotting. A luciferase reporter experiment was used in HEK293T cells to verify the interaction of miR-384-5p with GABRB1.</p><p><strong>Results: </strong>Ketamine induced neurotoxicity and miR-384-5p upregulation in hippocampal neurons. miR-384-5p downregulation mitigated ketamine-induced neurotoxicity by restraining apoptosis and ROS activity in neurons. GABRB1 was demonstrated to be targeted by miR-384-5p. GABRB1 depletion worsened ketamine-induced neurotoxicity. Moreover, GABRB1 depletion lessened the protective effect of miR-384-5p inhibition against ketamine-mediated neurotoxicity.</p><p><strong>Conclusion: </strong>miR-384-5p regulates ketamine-induced neurotoxicity in hippocampal neurons by targeting GABRB1.</p>","PeriodicalId":23395,"journal":{"name":"Turkish neurosurgery","volume":null,"pages":null},"PeriodicalIF":0.9000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"MiRNA-384-5p Targets GABRB1 to Regulate Ketamine-Induced Neurotoxicity in Neurons.\",\"authors\":\"Qiange Yang, Feiyu Long\",\"doi\":\"10.5137/1019-5149.JTN.36367-21.2\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Aim: </strong>To determine the function of miR-384-5p in ketamine-induced neurotoxicity.</p><p><strong>Material and methods: </strong>Neonatal hippocampal neurons were isolated from rats and treated with varying doses of ketamine. RT-qPCR was utilized to measure the miR-384-5p level in ketamine-treated neurons. Neuronal viability was evaluated by MTT assay. TUNEL staining and flow cytometry were applied to measure neuronal apoptosis. H2-DCFDA staining was utilized to detect the intracellular ROS level. Protein levels were measured using Western blotting. A luciferase reporter experiment was used in HEK293T cells to verify the interaction of miR-384-5p with GABRB1.</p><p><strong>Results: </strong>Ketamine induced neurotoxicity and miR-384-5p upregulation in hippocampal neurons. miR-384-5p downregulation mitigated ketamine-induced neurotoxicity by restraining apoptosis and ROS activity in neurons. GABRB1 was demonstrated to be targeted by miR-384-5p. GABRB1 depletion worsened ketamine-induced neurotoxicity. Moreover, GABRB1 depletion lessened the protective effect of miR-384-5p inhibition against ketamine-mediated neurotoxicity.</p><p><strong>Conclusion: </strong>miR-384-5p regulates ketamine-induced neurotoxicity in hippocampal neurons by targeting GABRB1.</p>\",\"PeriodicalId\":23395,\"journal\":{\"name\":\"Turkish neurosurgery\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.9000,\"publicationDate\":\"2024-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Turkish neurosurgery\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.5137/1019-5149.JTN.36367-21.2\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"CLINICAL NEUROLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Turkish neurosurgery","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.5137/1019-5149.JTN.36367-21.2","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
MiRNA-384-5p Targets GABRB1 to Regulate Ketamine-Induced Neurotoxicity in Neurons.
Aim: To determine the function of miR-384-5p in ketamine-induced neurotoxicity.
Material and methods: Neonatal hippocampal neurons were isolated from rats and treated with varying doses of ketamine. RT-qPCR was utilized to measure the miR-384-5p level in ketamine-treated neurons. Neuronal viability was evaluated by MTT assay. TUNEL staining and flow cytometry were applied to measure neuronal apoptosis. H2-DCFDA staining was utilized to detect the intracellular ROS level. Protein levels were measured using Western blotting. A luciferase reporter experiment was used in HEK293T cells to verify the interaction of miR-384-5p with GABRB1.
Results: Ketamine induced neurotoxicity and miR-384-5p upregulation in hippocampal neurons. miR-384-5p downregulation mitigated ketamine-induced neurotoxicity by restraining apoptosis and ROS activity in neurons. GABRB1 was demonstrated to be targeted by miR-384-5p. GABRB1 depletion worsened ketamine-induced neurotoxicity. Moreover, GABRB1 depletion lessened the protective effect of miR-384-5p inhibition against ketamine-mediated neurotoxicity.
Conclusion: miR-384-5p regulates ketamine-induced neurotoxicity in hippocampal neurons by targeting GABRB1.
期刊介绍：
Turkish Neurosurgery is a peer-reviewed, multidisciplinary, open access and totally free journal directed at an audience of neurosurgery physicians and scientists. The official language of the journal is English. The journal publishes original articles in the form of clinical and basic research. Turkish Neurosurgery will only publish studies that have institutional review board (IRB) approval and have strictly observed an acceptable follow-up period. With the exception of reference presentation, Turkish Neurosurgery requires that all manuscripts be prepared in accordance with the Uniform Requirements for Manuscripts Submitted to Biomedical Journals.
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