Department of Pain Clinic, Yantaishan Hospital, Yantai, Shandong Province, China.
Department of Pharmacy, The People's Hospital of Zhangqiu Area, Jinan, Shandong Province, China.
J Biol Regul Homeost Agents. 2020 May-Jun;34(3):893-900. doi: 10.23812/20-148-A-33.
Previous studies have shown that lncRNAs play crucial roles in cerebral ischemia/reperfusion injury. In this study, the function and possible mechanism of lncRNA HCP5 in cerebral ischemia/reperfusion injury was investigated. An oxygen glucose deprivation (OGD) model in N2a cells was used to simulate cerebral ischemia/reperfusion injury in vitro. The functional mechanism of lncRNA HCP5 was detected using Trypan blue staining, JC-1, MTT and dual luciferase reporter assays. The expression of apoptosis-related proteins (Bcl-2 and Bax) was measured by Western blot analysis. We found that lncRNA HCP5 was upregulated in N2a cells treated with OGD/R, and knockdown of lncRNA HCP5 enhanced cell viability and reduced cell death. In addition, miR-652-3p was found to act as a sponge for lncRNA HCP5. The overexpression of miR- 652-3p can prevent cerebral ischemic reperfusion injury, however, lncRNA HCP5 attenuated the protective effect of miR-652-3p in cerebral ischemic reperfusion injury. In conclusion, upregulation of lncRNA HCP5 may exacerbate cerebral ischemic reperfusion injury by sponging miR-652-3p.
先前的研究表明，长链非编码 RNA（lncRNAs）在脑缺血/再灌注损伤中发挥着关键作用。本研究旨在探讨 lncRNA HCP5 在脑缺血/再灌注损伤中的功能及其可能的作用机制。通过建立 N2a 细胞氧葡萄糖剥夺（OGD）模型来模拟体外脑缺血/再灌注损伤。采用台盼蓝染色、JC-1、MTT 和双荧光素酶报告基因检测等方法检测 lncRNA HCP5 的功能机制。通过 Western blot 分析检测凋亡相关蛋白（Bcl-2 和 Bax）的表达。结果发现，OGD/R 处理后的 N2a 细胞中 lncRNA HCP5 表达上调，lncRNA HCP5 敲低可提高细胞活力，减少细胞死亡。此外，发现 miR-652-3p 可作为 lncRNA HCP5 的海绵分子。过表达 miR-652-3p 可以预防脑缺血再灌注损伤，但 lncRNA HCP5 减弱了 miR-652-3p 在脑缺血再灌注损伤中的保护作用。综上所述，lncRNA HCP5 的上调可能通过海绵吸附 miR-652-3p 加重脑缺血再灌注损伤。
