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The SNHG10-miR-495-3p-PTEN axis is involved in sevoflurane-mediated protective effects in cardiomyocytes against hypoxia/reoxygenation injury

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资源类型：
WOS体系：
Pubmed体系：

收录情况： ◇ SCIE

作者：
He Jiandong[1,2] * ; Yu Jing[1,2] ; Han Chongfang[1,2,*1] ; Yang Wenqu[1,2] ; Zhang Chunmin[1,2] ; Hao Weihong[1,2] ; Duan Yinlei[1,2] ;
单位： [1]Department of Anesthesiology, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan 030032, Shanxi, China [2]Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei, China.
出处：
DOI： 10.1016/j.tiv.2023.105724
ISSN：

关键词： Sevoflurane SNHG10 miR-495-3p PTEN Cardiomyocyte Hypoxia

摘要：
Myocardial infarction (MI) has been considered a leading cause of death worldwide. Relieving ischemia-reperfusion myocardial damage is one of the major roles in treating MI. Sevoflurane postconditioning provides myocardial protection, and this study probes the mechanism of sevoflurane-mediated protective effects. A hypoxia/reoxygenation (H/R) model was constructed in cardiomyocytes, which were pretreated with 2.4% sevoflurane. Alterations in SNHG10, miR-495-3p, and PTEN levels were determined, and gain- or loss-of functional assays were conducted to confirm the role of the SNHG10/miR-495-3p axis, which is potentially regulated by sevoflurane. Cell viability, oxidative stress, and inflammatory reactions were all evaluated. The results indicated that sevoflurane post-conditioning attenuated H/R-induced cardiomyocyte damage and reduced the SHNH10 level. SNHG10 overexpression reversed sevoflurane-mediated protective effects on cardiomyocytes. Moreover, SNHG10 targeted miR-495-3p and restrained its expression, while miR-495-3p targeted PTEN, suppressed PTEN levels, and promoted HIF-1α expression. miR-495-3p overexpression decreased SNHG10-mediated myocardial injury and enhanced HIF-1α levels. However, no additional protection was found when sevoflurane was administered to H/R-exposed cardiomyocytes following treatment with the HIF-1α inhibitor LW6. Overall, sevoflurane protects cardiomyocytes from H/R by modulating the SNHG10-miR-495-3p-PTEN-HIF-1α axis.Copyright © 2023. Published by Elsevier Ltd.

基金：
Outstanding Youth Starting Fund of Shanxi Bethune Hospital (2019YJ11).
语种：
外文
WOS：
PubmedID：
中科院(CAS)分区：
出版当年[2023]版：
大类 | 3 区 医学
小类 | 3 区 毒理学
最新[2025]版：
大类 | 4 区 医学
小类 | 4 区 毒理学
JCR分区：
出版当年[2022]版：
Q2 TOXICOLOGY
最新[2023]版：
Q3 TOXICOLOGY

影响因子： 最新[2023版] 最新五年平均 出版当年[2022版] 出版当年五年平均 出版前一年[2021版] 出版后一年[2023版]

第一作者：
第一作者单位： [1]Department of Anesthesiology, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan 030032, Shanxi, China [2]Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei, China.
通讯作者：
通讯机构： [1]Department of Anesthesiology, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan 030032, Shanxi, China [2]Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei, China. [*1]Department of Anesthesiology, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, 99 Longcheng Street, xiaodian district, Taiyuan 030032, Shanxi, China
推荐引用方式(GB/T 7714)：
He Jiandong,Yu Jing,Han Chongfang,et al.The SNHG10-miR-495-3p-PTEN axis is involved in sevoflurane-mediated protective effects in cardiomyocytes against hypoxia/reoxygenation injury[J].TOXICOLOGY IN VITRO.2024,94:105724.doi:10.1016/j.tiv.2023.105724.
APA：
He Jiandong,Yu Jing,Han Chongfang,Yang Wenqu,Zhang Chunmin...&Duan Yinlei.(2024).The SNHG10-miR-495-3p-PTEN axis is involved in sevoflurane-mediated protective effects in cardiomyocytes against hypoxia/reoxygenation injury.TOXICOLOGY IN VITRO,94,
MLA：
He Jiandong,et al."The SNHG10-miR-495-3p-PTEN axis is involved in sevoflurane-mediated protective effects in cardiomyocytes against hypoxia/reoxygenation injury".TOXICOLOGY IN VITRO 94.(2024):105724

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