LINC00665 knockdown protects against cerebral ischemia-reperfusion injury

被引:0
|
作者
Yan, T-H [1 ]
Ma, C-H [2 ]
Peng, N. [3 ]
Li, Y-E [4 ]
Li, Q-Y [5 ]
Wang, H. [6 ]
机构
[1] Zhangqiu Dist Peoples Hosp, Dept Crit Care Med, Jinan, Peoples R China
[2] Qingdao Municipal Hosp, Clin Skills Training Ctr, Qingdao, Peoples R China
[3] Zhangqiu Dist Peoples Hosp, Operat Room, Jinan, Peoples R China
[4] Zhangqiu Dist Peoples Hosp, Dept Med, Jinan 250200, Peoples R China
[5] Zhangqiu Dist People Hosp, Image Ctr, Jinan, Peoples R China
[6] Third Peoples Hosp Qingdao, Dept Anesthesiol, 29 Yongping Rd, Qingdao 266000, Peoples R China
关键词
LINC00665; miR-744-5p; cerebral ischemia-reperfusion injury; APOPTOSIS;
D O I
暂无
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
LINC00665 has been reported to participate in several human diseases. However, the role of LINC00665 in cerebral ischemia-reperfusion (CI/R) is still unknown. This study is designed to investigate the role of LINC00665 in rats with CI/R injury. We established middle cerebral artery occlusion/reperfusion (MCAO/R) rats model in vivo. PC12 cells treated with oxygen-glucose deprivation/reperfusion (OGD/R) were used to establish in vitro I/R model. RT-qPCR assay was adopted to assess the mRNA expression of LINC00665 and miR-744-5p. MTT assay was used to determine cell viability. The protein expression of Bax and Bcl-2 were detected by Western blot assay. The relationship between LINC00665 and miR-744-5p was confirmed by dual luciferase reporter assay and RNA immunoprecipitation (RIP). In this study, we found that LINC00665 was sharply up regulated in MCAO/R rats and PC12 cells treated with I/R. Functionally, LINC00665 knockdown attenuated oxidative damage in PC12 cells treated with I/R. Moreover, LINC00665 knockdown promoted cell viability, while inhibited cell apoptosis in PC12 cells treated with I/R. In addition, miR-744-5p was confirmed to be a target of LINC00665. LINC00665 knockdown was validated to project CI/R injury by sponging miR-744-5p expression.
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页码:51 / 58
页数:8
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