Effects of Long Noncoding RNA H19 on Isoflurane-Induced Cognitive Dysregulation by Promoting Neuroinflammation.

IF 2.2 4区医学 Q3 ENDOCRINOLOGY & METABOLISM

Neuroimmunomodulation Pub Date : 2022-01-01 Epub Date: 2021-12-02 DOI:10.1159/000519124

Yanhu Ge, Duomao Lin, Boqun Cui, Liang Zhang, Shurong Li, Zhaoqi Wang, Jun Ma

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引用次数: 7

Abstract

Introduction: Isoflurane (ISO) may cause neuronal apoptosis and synaptic disorder during development, and damage long-term learning and memory function. This observation aimed to study the function of H19 in vitro and in vivo tests and the further mechanism was identified.

Methods: ISO cell models and rat models were established and reactive oxygen species (ROS) identified. The viability and apoptosis of HT22 cells were detected by the MTT and flow cytometer. Morris water maze test was conducted to analyze the neurotoxicity of ISO on spatial learning and memory ability. Quantitative PCR was the method to verify the expression of H19. The concentration of inflammatory indicators was identified by enzyme-linked immunosorbent assay.

Results: 1.5% and 2% ISO led to the neurotoxicity of HT22 cells and increased expression of H19. Silenced H19 meliorated these adverse impacts of ISO. Interference of H19 exerted neuroprotective roles by repressing modified neurological severity score, inhibiting escape latency, elevating distance and time of target area, and controlling ROS and inflammation. MiR-17-5p might be a promising competing endogenous RNA of H19. The expression of miR-17-5p was reduced in the ISO group and reversed by the absence of H19.

Conclusion: Our results of in vitro and in vivo assay indicated that the absence of HT22 is a neuroprotective regulator of cognition and inflammation by accumulating miR-17-5p.

查看原文本刊更多论文

长链非编码RNA H19通过促进神经炎症对异氟醚诱导的认知失调的影响。

简介:异氟醚可引起发育过程中神经元凋亡和突触紊乱，损害长期学习记忆功能。本研究旨在通过体外和体内实验研究H19的功能，并进一步确定其作用机制。方法:建立ISO细胞模型和大鼠模型，鉴定活性氧(ROS)。采用MTT和流式细胞仪检测HT22细胞活力和凋亡情况。采用Morris水迷宫实验分析ISO对大鼠空间学习记忆能力的神经毒性。采用定量PCR方法验证H19的表达。采用酶联免疫吸附法测定炎症指标的浓度。结果:1.5%和2% ISO可引起HT22细胞的神经毒性，并增加H19的表达。沉默的H19改善了ISO的这些不利影响。H19的干扰通过抑制改良神经系统严重程度评分、抑制逃避潜伏期、提高靶区距离和时间、控制ROS和炎症等发挥神经保护作用。MiR-17-5p可能是一种有前景的H19竞争内源性RNA。miR-17-5p的表达在ISO组中降低，并因缺乏H19而逆转。结论:我们的体外和体内实验结果表明，HT22的缺失是通过积累miR-17-5p来调节认知和炎症的神经保护因子。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Neuroimmunomodulation 医学-免疫学

CiteScore

3.60

自引率

4.20%

发文量

审稿时长

>12 weeks

期刊介绍： The rapidly expanding area of research known as neuroimmunomodulation explores the way in which the nervous system interacts with the immune system via neural, hormonal, and paracrine actions. Encompassing both basic and clinical research, ''Neuroimmunomodulation'' reports on all aspects of these interactions. Basic investigations consider all neural and humoral networks from molecular genetics through cell regulation to integrative systems of the body. The journal also aims to clarify the basic mechanisms involved in the pathogenesis of the CNS pathology in AIDS patients and in various neurodegenerative diseases. Although primarily devoted to research articles, timely reviews are published on a regular basis.