{"title":"敲除长非编码RNA CRNDE通过mir-489-3p/FOXO3途径减轻缺血再灌注诱导的脑损伤中的细胞凋亡和炎症。","authors":"Yinbao Hu, Min Li","doi":"10.5137/1019-5149.JTN.36652-21.2","DOIUrl":null,"url":null,"abstract":"<p><strong>Aim: </strong>To examine the role and mechanism of colorectal tumor differential expression (CRNDE) in brain injury induced by ischemicreperfusion.</p><p><strong>Material and methods: </strong>Sh-SY5Y cells were cultured, and oxygen and glucose deprivation/reperfusion (OGD/R) injury tests were performed. The effects on SH-SY5Y cells were evaluated by the Cell Counting Kit-8 (CCK-8) assay, qPCR, apoptosis analysis, western blot analysis, ELISA, a luciferase reporter assay, and an RNA pull-down assay.</p><p><strong>Results: </strong>Knockdown of CRBDE ameliorated SH-SY5Y cell impairment induced by OGD/R. CRNDE, the target of mir-489-3p, was directly bound to FOXO3. Mir-489-3p knockdown partially reversed OGD/R-mediated impairment in CRBDE knockdown SH-SY5Y cells.</p><p><strong>Conclusion: </strong>The results indicate that knockdown of lncRNA CRNDE ameliorates apoptosis and the inflammatory response in ischemia-reperfusion-induced brain injury through the mir-489-3p/FOXO3 axis. LncRNA CRNDE may represent a novel therapeutic target for brain injury.</p>","PeriodicalId":94381,"journal":{"name":"Turkish neurosurgery","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Knockdown of the Long Noncoding RNA CRNDE Ameliorates Apoptosis and Inflammation in Ischemia-Reperfusion-Induced Brain Injury via the mir-489-3p/FOXO3 Pathway.\",\"authors\":\"Yinbao Hu, Min Li\",\"doi\":\"10.5137/1019-5149.JTN.36652-21.2\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Aim: </strong>To examine the role and mechanism of colorectal tumor differential expression (CRNDE) in brain injury induced by ischemicreperfusion.</p><p><strong>Material and methods: </strong>Sh-SY5Y cells were cultured, and oxygen and glucose deprivation/reperfusion (OGD/R) injury tests were performed. The effects on SH-SY5Y cells were evaluated by the Cell Counting Kit-8 (CCK-8) assay, qPCR, apoptosis analysis, western blot analysis, ELISA, a luciferase reporter assay, and an RNA pull-down assay.</p><p><strong>Results: </strong>Knockdown of CRBDE ameliorated SH-SY5Y cell impairment induced by OGD/R. CRNDE, the target of mir-489-3p, was directly bound to FOXO3. Mir-489-3p knockdown partially reversed OGD/R-mediated impairment in CRBDE knockdown SH-SY5Y cells.</p><p><strong>Conclusion: </strong>The results indicate that knockdown of lncRNA CRNDE ameliorates apoptosis and the inflammatory response in ischemia-reperfusion-induced brain injury through the mir-489-3p/FOXO3 axis. LncRNA CRNDE may represent a novel therapeutic target for brain injury.</p>\",\"PeriodicalId\":94381,\"journal\":{\"name\":\"Turkish neurosurgery\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2023-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Turkish neurosurgery\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.5137/1019-5149.JTN.36652-21.2\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Turkish neurosurgery","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5137/1019-5149.JTN.36652-21.2","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Knockdown of the Long Noncoding RNA CRNDE Ameliorates Apoptosis and Inflammation in Ischemia-Reperfusion-Induced Brain Injury via the mir-489-3p/FOXO3 Pathway.
Aim: To examine the role and mechanism of colorectal tumor differential expression (CRNDE) in brain injury induced by ischemicreperfusion.
Material and methods: Sh-SY5Y cells were cultured, and oxygen and glucose deprivation/reperfusion (OGD/R) injury tests were performed. The effects on SH-SY5Y cells were evaluated by the Cell Counting Kit-8 (CCK-8) assay, qPCR, apoptosis analysis, western blot analysis, ELISA, a luciferase reporter assay, and an RNA pull-down assay.
Results: Knockdown of CRBDE ameliorated SH-SY5Y cell impairment induced by OGD/R. CRNDE, the target of mir-489-3p, was directly bound to FOXO3. Mir-489-3p knockdown partially reversed OGD/R-mediated impairment in CRBDE knockdown SH-SY5Y cells.
Conclusion: The results indicate that knockdown of lncRNA CRNDE ameliorates apoptosis and the inflammatory response in ischemia-reperfusion-induced brain injury through the mir-489-3p/FOXO3 axis. LncRNA CRNDE may represent a novel therapeutic target for brain injury.
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