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ArticleNeurochemical research2025

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

Jing Qian, Xiaoxiao Dai, Zhaoxuan Li

Abstract read
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Article in Neurochemical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Jing Qian *Department of Anesthesiology, Yancheng Third People's Hospital, Yancheng City, Jiangsu Province, China.
Xiaoxiao Dai *The Armed Police Corps Hospital of Anhui, Hefei City, Anhui Province, China.
Zhaoxuan LiDepartment of Anesthesiology, Union Hospital Tongji Medical College Huazhong University of Science and Technology, No.1277, Jiefang Avenue, Wuhan City, Hubei Province, China. Lizhaoxuan_whuh@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Anesthetics, InhalationCognitive DysfunctionMicroRNAsOxidative StressRNA, Long NoncodingSevofluraneAnimalsApoptosisCell LineGene SilencingHippocampusMaleMiceRatsRats, Sprague-DawleyAnesthetics, InhalationMicroRNAsRNA, Long NoncodingSevofluraneCognitive dysfunctionmiR-486-5pOxidative stressPVT1Sevoflurane

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.