Knockdown of the Long Noncoding RNA CRNDE Ameliorates Apoptosis and Inflammation in Ischemia-Reperfusion-Induced Brain Injury via the mir-489-3p/FOXO3 Pathway.
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Abstract
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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