Protective effects of miRNA-589 on cerebral ischemia-reperfusion injury

被引:2
作者
Ma, G-P [1 ]
Yang, B-Z [2 ]
Zhang, Y-S [1 ]
Wang, B. [1 ]
Wei, X-H [1 ]
Zhang, R-F [1 ]
Jia, K-H [1 ]
Gao, J-P [1 ]
机构
[1] First Hosp Tianshui, Dept Neurol, 105 Jianshe Rd, Tianshui 741000, Gansu, Peoples R China
[2] First Hosp Tianshui, Dept Special Needs Diag & Treatment, Tianshui, Peoples R China
关键词
MiRNA-589; cerebral IRI; BV2; TRAF6; inflammation; BRAIN; INFLAMMATION; STROKE; BLOOD; EXPRESSION; MICRORNA; TRAF6;
D O I
暂无
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
To uncover the potential influence of microRNA-589 (miRNA-589) on cerebral ischemia-reperfusion injury (IRI) and the underlying mechanism, BV2 cells were stimulated by lipopolysaccharide (LPS) or conditioned medium (CM) of primary cortical neurons undergoing oxygen-glucose deprivation (OGD). Regulatory effects of miRNA-589 on the release of inflammatory factors in BV2 cells induced with LPS or CM of primary cortical neurons undergoing OGD were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA). The interaction between miRNA-589 and TRAF6 was finally assessed by dual-luciferase reporter gene assay. MiRNA-589 was downregulated in BV2 cells induced with LPS or CM of primary cortical neurons undergoing OGD. Overexpression of miRNA-589 reduced the release of inflammatory factors in LPS or CM-induced BV2 cells. TRAF6 was verified to be the downstream gene of miRNA-589, and its level was negatively regulated by miRNA-589. MiRNA-589 is downregulated following cerebral IRI and alleviates inflammatory response through negatively regulating TRAF6.
引用
收藏
页码:1269 / 1275
页数:7
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