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Silencing PVT1 Alleviates Sevoflurane Anesthesia-Induced Oxidative Stress and Cognitive Dysfunction by Regulating
Jing Qian1,2, Xiaoxiao Dai3, Zhaoxuan Li4
1Department of Anesthesiology, Yancheng Third People's Hospital, Yancheng City, Jiangsu Province, China.
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.
Insights
Long non-coding RNA PVT1 exacerbates sevoflurane-induced oxidative stress and cognitive dysfunction by targeting miR-486-5p. Silencing PVT1 offers a potential therapeutic strategy for sevoflurane-induced nerve injury.
Area of Science:
- Neuroscience
- Molecular Biology
- Anesthesiology
Background:
- Sevoflurane anesthesia can induce oxidative stress and cognitive dysfunction.
- Long non-coding RNAs (lncRNAs) are implicated in various cellular processes, including neuronal injury.
Purpose of the Study:
- To investigate the role of lncRNA PVT1 in sevoflurane-induced oxidative stress and cognitive dysfunction.
- To elucidate the underlying molecular mechanism involving microRNA (miRNA) interactions.
Main Methods:
- Quantitative real-time PCR (RT-qPCR) for gene expression analysis.
- MTT assay and flow cytometry for cell viability and apoptosis.
- Biochemical assays for oxidative stress markers (MDA, ROS, SOD).
- Morris water maze (MWM) test for cognitive function assessment.
- Bioinformatic prediction, dual-luciferase reporter, and RNA immunoprecipitation (RIP) assays for miRNA targeting verification.
Main Results:
- PVT1 expression was significantly upregulated in response to sevoflurane exposure in both rat hippocampal tissues and HT22 cells.
- Silencing PVT1 ameliorated sevoflurane-induced apoptosis, oxidative stress, and cognitive deficits.
- PVT1 was found to directly target miR-486-5p.
- Inhibition of miR-486-5p reversed the protective effects of PVT1 silencing, worsening sevoflurane-induced neuronal damage.
Conclusions:
- PVT1 plays a critical role in promoting sevoflurane-induced oxidative stress and cognitive impairment.
- The PVT1/miR-486-5p axis is a key mechanism underlying sevoflurane neurotoxicity.
- Targeting PVT1 may represent a novel therapeutic approach for mitigating sevoflurane-induced nerve injury.
