本研究主要探讨miR-652-3p在异氟烷（ISO）对心肌缺血再灌注（I/R）损伤的保护作用中的作用和机制。 H9c2细胞经过不同浓度的ISO预处理，随后构建缺氧/复氧（H/R）模型。通过逆转录聚合酶链反应 (RT-qPCR) 评估 miR-652-3p、ISL LIM 同源框 1 (ISL1) 以及炎症细胞因子白细胞介素 (IL)-6 和肿瘤坏死因子-α (TNF-α) 的水平。采用酶联免疫吸附测定法来研究心肌损伤标志物的浓度，例如肌酸激酶-MB (CK-MB) 和心肌肌钙蛋白 I (cTnI)。使用细胞计数试剂盒-8评估细胞活力，使用流式细胞术测量细胞凋亡。此外，还进行了双荧光素酶报告基因测定以验证 ISL1 和 miR-652-3p 之间的靶向关系。在此，我们证实，随着缺氧时间的延长，miR-652-3p 的水平逐渐升高；然而，ISO 预处理抑制了这种增加（P<0.05）。此外，ISO预处理可防止H/R诱导的细胞活力下降、细胞凋亡增加以及IL-6、TNF-α、CK-MB和cTnI的过量产生（P<0.05）。然而，ISO 的抑制作用被 miR-652-3p 水平的增加所抵消（P<0.05）。 ISL1 是 miR-652-3p 的潜在靶标。与对照相比，H/R 诱导抑制了 ISL1 水平，但 ISO 处理增加了其表达 (P < 0.05)。 ISL1的过表达抑制了ISO对miR-652-3p升高引起的心肌损伤的保护作用的消除（P < 0.05）。本研究的结果证实，miR-652-3p 通过靶向 ISL1 减弱 ISO 对心肌缺血中心肌细胞的保护作用。© 2024。作者获得 Springer Science Business Media, LLC（Springer 旗下公司）的独家许可自然。

This research is concentrated on investigating the role and mechanism of miR-652-3p in the protective effects of isoflurane (ISO) against myocardial ischemia-reperfusion (I/R) injury. H9c2 cells underwent pretreatment with varying concentrations of ISO, and subsequently, a hypoxia/reoxygenation (H/R) model was constructed. The levels of miR-652-3p, ISL LIM homeobox 1 (ISL1), and inflammatory cytokines interleukin (IL)-6 and tumor necrosis factor-alpha (TNF-α) were evaluated through reverse transcription polymerase chain reaction (RT-qPCR). Enzyme-linked immunosorbent assay was employed to investigate concentrations of myocardial injury markers, such as creatine kinase-MB (CK-MB) and cardiac troponin I (cTnI). Cell counting kit-8 was used to evaluate cell viability, while flow cytometry was utilized to measure apoptosis. Additionally, a dual luciferase reporter assay was conducted to validate the targeting relationship between ISL1 and miR-652-3p. Herein, we confirmed that the level of miR-652-3p was gradually increased with prolonged hypoxia; nevertheless, this increase was suppressed by ISO pretreatment (P < 0.05). Additionally, ISO pretreatment prevented the decrease in cell viability, increase in apoptosis, and overproduction of IL-6, TNF-α, CK-MB, and cTnI induced by H/R (P < 0.05). However, the inhibitory effects of ISO were counteracted by the increased levels of miR-652-3p (P < 0.05). ISL1 is a potential target of miR-652-3p. H/R induction suppressed ISL1 levels compared to the control, but ISO treatment increased its expression (P < 0.05). Overexpression of ISL1 inhibited the elimination of the protective effect of ISO on myocardial damage induced by the elevation of miR-652-3p (P < 0.05). The findings of this research confirm that miR-652-3p attenuated the protective effect of ISO on cardiomyocytes in myocardial ischemia by targeting ISL1.© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.