Department of Neurology, The Third Affiliated Hospital of Qiqihar Medical University, Ward 3, Qiqihar 161000, China.
President's Office, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar 161000, China.
J Healthc Eng. 2021 Nov 26;2021:6577799. doi: 10.1155/2021/6577799. eCollection 2021.
Ischemic stroke is a kind of disease with high mortality and high disability, which brings a huge burden to the public health system (Hu et al. (2017)), and it poses a serious threat to the quality of life of patients. Cerebral ischemia/reperfusion injury is an important pathophysiological mechanism. This study aims to assess the mechanism of SNHG15 in the occurrence and development of cerebral ischemia/reperfusion injury of nerve cells and to investigate its potential value for diagnosis and treatment. SNHG15 targeted miRNA molecules and target genes were predicted with bioinformatics tools such as StarBase and TargetScan. The process of ischemic reperfusion in cerebral apoplexy in normal cultured and oxygen-glucose-deprived and reoxygenated neurons was simulated with RT-PCR and western blot technique. The expressions of SNHG15 and miR-141 were detected with qPCR, and the expressions of SIRT1 and p65, TNF-, ROS, iNOS, and IL-6 were detected with western blot. Meanwhile, SNHG15 siRNAs and miR-141 mimics were transfected for SH-SY5Y, with western blot testing. And the expressions of miR-141, SIRT1, and p65, TNF-, ROS, iNOS, and IL-6 were tested. According to the prediction with bioinformatics tools of StarBase and TargetScan, miR-141 is the target of lncSNHG15. In the luciferase reporter plasmid double-luciferase assay, miR-141 and SIRT1 were defined as the target relationship. In the oxygen-glucose-deprived reoxygenation model group, SNHG15 expression increased, miR-141 expression decreased, SIRT1 expression increased, and the expressions of p65, TNF-, ROS, iNOS, and IL-6 decreased. In the SNHG15-siRNA-transfected oxygen-glucose-deprived reoxygenation cell model group, miR-141 expression increased, SIRT1 expression decreased, and the expressions of p65, TNF-, and IL-6 increased compared with the si-NC group. In the miR-141-mimic-transfected oxygen-glucose-deprived reoxygenation cell model, SNHG15 expression decreased, SIRT1 expression decreased, and the expressions of p65, TNF-, IL-1, and IL-6 increased. In conclusion, SNHG15 expression increased during the process of oxygen-glucose-deprived reoxygenation, and the oxidative stress process was reduced by miR-141/SIRT1.
缺血性脑卒中是一种死亡率和高残疾率的疾病,给公共卫生系统带来了巨大的负担(Hu 等人,2017 年),严重威胁着患者的生活质量。脑缺血再灌注损伤是一种重要的病理生理机制。本研究旨在评估 SNHG15 在神经细胞脑缺血再灌注损伤发生发展中的作用机制,并探讨其在诊断和治疗中的潜在价值。使用生物信息学工具 StarBase 和 TargetScan 预测 SNHG15 靶向的 miRNA 分子和靶基因。通过 RT-PCR 和 Western blot 技术模拟脑中风中正常培养和氧葡萄糖剥夺及再氧合神经元的缺血再灌注过程。用 qPCR 检测 SNHG15 和 miR-141 的表达,用 Western blot 检测 SIRT1 和 p65、TNF-、ROS、iNOS 和 IL-6 的表达。同时,用 SNHG15 siRNAs 和 miR-141 模拟物转染 SH-SY5Y,用 Western blot 检测 miR-141、SIRT1 和 p65、TNF-、ROS、iNOS 和 IL-6 的表达。根据生物信息学工具 StarBase 和 TargetScan 的预测,miR-141 是 lncSNHG15 的靶基因。在荧光素酶报告质粒双荧光素酶测定中,miR-141 和 SIRT1 被定义为靶关系。在氧葡萄糖剥夺再氧合模型组中,SNHG15 表达增加,miR-141 表达减少,SIRT1 表达增加,p65、TNF-、ROS、iNOS 和 IL-6 的表达减少。在 SNHG15-siRNA 转染的氧葡萄糖剥夺再氧合细胞模型组中,与 si-NC 组相比,miR-141 表达增加,SIRT1 表达减少,p65、TNF-和 IL-6 的表达增加。在 miR-141 模拟物转染的氧葡萄糖剥夺再氧合细胞模型中,SNHG15 表达减少,SIRT1 表达减少,p65、TNF-、IL-1 和 IL-6 的表达增加。综上所述,在氧葡萄糖剥夺再氧合过程中 SNHG15 表达增加,miR-141/SIRT1 减少氧化应激过程。