Silencing PVT1 Alleviates Sevoflurane Anesthesia-Induced Oxidative Stress and Cognitive Dysfunction by Regulating miR-486-5p

IF 3.8 3区医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Neurochemical Research Pub Date : 2025-09-11 DOI:10.1007/s11064-025-04537-1

Jing Qian, Xiaoxiao Dai, Zhaoxuan Li

{"title":"Silencing PVT1 Alleviates Sevoflurane Anesthesia-Induced Oxidative Stress and Cognitive Dysfunction by Regulating miR-486-5p","authors":"Jing Qian, Xiaoxiao Dai, Zhaoxuan Li","doi":"10.1007/s11064-025-04537-1","DOIUrl":null,"url":null,"abstract":"<div><p>To investigate the role and mechanism of long non-coding RNA PVT1 in sevoflurane-induced oxidative stress and cognitive dysfunction. The expression level of PVT1 and the mRNA expressions of Caspase-3, Bax, and Bcl2 were detected by RT-qPCR. Cell viability and apoptosis rate were evaluated by MTT assay and flow cytometry, respectively. The levels of malondialdehyde (MDA), reactive oxygen species (ROS), and superoxide dismutase (SOD) were determined using commercial kits. The cognitive function of rats was assessed by Morris water maze (MWM) test. Online databases were used to predict the microRNAs (miRNAs) targeted by PVT1, and dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to verify the targeted binding relationship. PVT1 levels were significantly upregulated in hippocampal tissues of rats and HT22 cells treated with sevoflurane. Silencing of PVT1 effectively alleviated sevoflurane-induced cell apoptosis, oxidative stress, and cognitive dysfunction. Mechanistic studies showed that PVT1 targeted miR-486-5p. In sevoflurane-treated hippocampal tissues of rats and HT22 cells, inhibition of miR-486-5p counteracted the protective effects of PVT1 silencing, leading to increased cell apoptosis, exacerbated oxidative stress, and deteriorated cognitive dysfunction. PVT1 silencing mitigates oxidative stress response and cognitive dysfunction by targeting miR-486-5p, providing a novel research perspective for the treatment of sevoflurane-induced nerve injury.</p></div>","PeriodicalId":719,"journal":{"name":"Neurochemical Research","volume":"50 5","pages":""},"PeriodicalIF":3.8000,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neurochemical Research","FirstCategoryId":"3","ListUrlMain":"https://link.springer.com/article/10.1007/s11064-025-04537-1","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

To investigate the role and mechanism of long non-coding RNA PVT1 in sevoflurane-induced oxidative stress and cognitive dysfunction. The expression level of PVT1 and the mRNA expressions of Caspase-3, Bax, and Bcl2 were detected by RT-qPCR. Cell viability and apoptosis rate were evaluated by MTT assay and flow cytometry, respectively. The levels of malondialdehyde (MDA), reactive oxygen species (ROS), and superoxide dismutase (SOD) were determined using commercial kits. The cognitive function of rats was assessed by Morris water maze (MWM) test. Online databases were used to predict the microRNAs (miRNAs) targeted by PVT1, and dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to verify the targeted binding relationship. PVT1 levels were significantly upregulated in hippocampal tissues of rats and HT22 cells treated with sevoflurane. Silencing of PVT1 effectively alleviated sevoflurane-induced cell apoptosis, oxidative stress, and cognitive dysfunction. Mechanistic studies showed that PVT1 targeted miR-486-5p. In sevoflurane-treated hippocampal tissues of rats and HT22 cells, inhibition of miR-486-5p counteracted the protective effects of PVT1 silencing, leading to increased cell apoptosis, exacerbated oxidative stress, and deteriorated cognitive dysfunction. PVT1 silencing mitigates oxidative stress response and cognitive dysfunction by targeting miR-486-5p, providing a novel research perspective for the treatment of sevoflurane-induced nerve injury.

查看原文本刊更多论文

沉默PVT1通过调节miR-486-5p减轻七氟醚麻醉诱导的氧化应激和认知功能障碍

探讨长链非编码RNA PVT1在七氟醚诱导氧化应激和认知功能障碍中的作用及机制。RT-qPCR检测PVT1表达水平及Caspase-3、Bax、Bcl2 mRNA表达水平。分别用MTT法和流式细胞术检测细胞活力和凋亡率。丙二醛（MDA）、活性氧（ROS）和超氧化物歧化酶（SOD）水平采用商用试剂盒测定。采用Morris水迷宫（Morris water maze， MWM）测试大鼠认知功能。利用在线数据库预测PVT1靶向的microRNAs (miRNAs)，并通过双荧光素酶报告基因实验和RNA免疫沉淀（RIP）实验验证PVT1靶向结合关系。七氟醚处理大鼠海马组织和HT22细胞中PVT1水平显著上调。PVT1沉默可有效缓解七氟醚诱导的细胞凋亡、氧化应激和认知功能障碍。机制研究表明PVT1靶向miR-486-5p。在七氟烷处理的大鼠海马组织和HT22细胞中，miR-486-5p的抑制抵消了PVT1沉默的保护作用，导致细胞凋亡增加，氧化应激加剧，认知功能障碍恶化。PVT1沉默通过靶向miR-486-5p减轻氧化应激反应和认知功能障碍，为七氟醚诱导的神经损伤的治疗提供了新的研究视角。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Neurochemical Research 医学-神经科学

CiteScore

7.70

自引率

2.30%

发文量

320

审稿时长

6 months

期刊介绍： Neurochemical Research is devoted to the rapid publication of studies that use neurochemical methodology in research on nervous system structure and function. The journal publishes original reports of experimental and clinical research results, perceptive reviews of significant problem areas in the neurosciences, brief comments of a methodological or interpretive nature, and research summaries conducted by leading scientists whose works are not readily available in English.