Neuroprotective Effect of HOTAIR Silencing on Isoflurane-Induced Cognitive Dysfunction via Sponging microRNA-129-5p and Inhibiting Neuroinflammation.

IF 2.2 4区医学 Q3 ENDOCRINOLOGY & METABOLISM

Neuroimmunomodulation Pub Date : 2022-01-01 DOI:10.1159/000521014

Ying Wang, Shanshan Zhao, Guohua Li, Dawei Wang, Yanwu Jin

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引用次数: 2

Abstract

Introduction: This article purposed to detect the function of the HOTAIR and HOTAIR/microRNA-129-5p (miR-129-5p) axis on the isoflurane (ISO)-injured cells and rat, and propounded a novel perspective in exploring the molecular pathogenesis of ISO damage.

Methods: The expression of HOTAIR and miR-129-5p was tested by quantitative real-time PCR. The viable cells were identified using MMT, and the apoptotic cells were provided by flow cytometry. The concentration of proinflammatory indicators was revealed by enzyme-linked immunosorbent assay kits. The function of HOTAIR on oxidative stress was detected by commercial kits. A luciferase assay was performed to confirm the relationship between miR-129-5p and HOTAIR. The Morris water maze test was conducted to elucidate the cognition of SD rats.

Results: The expression of HOTAIR was enhanced and the expression of miR-129-5p was lessened in the ISO-evoked SD rats and HT22 cells. The interference of HOTAIR reversed the injury of ISO on cell viability, apoptosis, inflammation, and oxidative stress. Besides, HOTAIR might be a target ceRNA of miR-129-5p. MiR-129-5p abrogated the function of silenced HOTAIR on cell viability, cell apoptosis, inflammation, and oxidative stress. Moreover, in vivo, the intervention of HOTAIR reversed the influence of ISO on cognition and oxidative stress by binding miR-129-5p.

Discussion/conclusion: Lowly expressed HOTAIR contributed to the recovery of the ISO-injured HT22 cell model from the abnormal viability, apoptosis, inflammation, and oxidative stress by regulating miR-129-5p. miR-129-5p mediated the function of HOTAIR on cognition and oxidative balance in the ISO-managed SD rat model.

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HOTAIR沉默对异氟醚诱导的认知功能障碍的神经保护作用通过海绵微rna -129-5p和抑制神经炎症。

简介:本文旨在检测HOTAIR和HOTAIR/microRNA-129-5p (miR-129-5p)轴在异氟醚(ISO)损伤细胞和大鼠中的功能，为探索ISO损伤的分子发病机制提供新的视角。方法:采用实时荧光定量PCR检测HOTAIR和miR-129-5p的表达。MMT法鉴定活细胞，流式细胞术检测凋亡细胞。酶联免疫吸附测定试剂盒检测促炎指标的浓度。采用商品化试剂盒检测HOTAIR对氧化应激的作用。荧光素酶测定证实miR-129-5p与HOTAIR之间的关系。采用Morris水迷宫实验研究SD大鼠的认知功能。结果:在iso诱发的SD大鼠和HT22细胞中，HOTAIR表达增强，miR-129-5p表达降低。HOTAIR的干扰可逆转ISO对细胞活力、凋亡、炎症和氧化应激的损伤。此外，HOTAIR可能是miR-129-5p的靶标ceRNA。MiR-129-5p消除了沉默的HOTAIR对细胞活力、细胞凋亡、炎症和氧化应激的作用。此外，在体内，HOTAIR的干预通过结合miR-129-5p逆转了ISO对认知和氧化应激的影响。讨论/结论:低表达的HOTAIR通过调节miR-129-5p参与了iso损伤HT22细胞模型从异常活力、凋亡、炎症和氧化应激中恢复的过程。在iso管理的SD大鼠模型中，miR-129-5p介导HOTAIR对认知和氧化平衡的功能。

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.