基因敲除
FOXO3公司
细胞凋亡
医学
SH-SY5Y型
免疫印迹
癌症研究
再灌注损伤
长非编码RNA
炎症
缺血
分子生物学
细胞培养
下调和上调
免疫学
生物
内科学
基因
生物化学
蛋白激酶B
遗传学
神经母细胞瘤
出处
期刊:Turkish Neurosurgery
[Turkish Neurosurgical Society]
日期:2022-01-01
标识
DOI:10.5137/1019-5149.jtn.36652-21.2
摘要
To examine the role and mechanism of colorectal tumor differential expression (CRNDE) in brain injury induced by ischemicreperfusion.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.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.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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