The protective effect and mechanism of isoflurane on myocardial injury was investigated by constructing in vitro hypoxia/reoxygenation (HR) cell model. HR cell models were established in vitro and treated with isoflurane (ISO). qRT-PCR was used to detect the relative expression of miR-18a-5p. CCK-8 kit and flow cytometry were performed to evaluate cell proliferation and apoptosis. The myocardial injury related markers, such as Cκ-MB, cTnI and LDH were detected by ELISA. Luciferase reporter gene assay was used to verify the interaction between miR-18a-5p and target genes. The expression of miR-18a-5p was significantly increased in hypoxic cardiomyocytes compared with control group (P < 0.001). Meanwhile, cardiomyocytes in the HR group showed inhibition of proliferation, a significant increase in cell apoptosis and in myocardial injury indicators, such as Cκ-MB, cTnI and LDH (P < 0.001). However, 1% ISO treatment alleviated myocardial cell injury induced by HR. Transfection of miR-18a-5p under ISO reduced the protective effect of 1% ISO against myocardial cell damage. Luciferase report gene assay confirmed that CCND2 might be the target gene of miR-18a-5p. In the in vitro cell model of myocardium, ISO alleviated cardiomyocyte injury caused by hypoxia/reoxygenation by down-regulating the expression of miR-18a-5p.

通过构建体外缺氧/复氧(HR)细胞模型，研究异氟醚对心肌损伤的保护作用及机制。HR 细胞模型在体外建立并用异氟醚 (ISO) 处理。qRT-PCR用于检测miR-18a-5p的相对表达。进行CCK-8试剂盒和流式细胞术以评估细胞增殖和凋亡。ELISA检测心肌损伤相关标志物Cκ-MB、cTnI、LDH。荧光素酶报告基因检测用于验证 miR-18a-5p 与靶基因之间的相互作用。与对照组相比，miR-18a-5p在缺氧心肌细胞中的表达显着升高（P < 0.001)。同时，HR组心肌细胞增殖受到抑制，细胞凋亡明显增加，Cκ-MB、cTnI、LDH等心肌损伤指标显着增加（P  < 0.001）。然而，1% ISO 治疗减轻了 HR 诱导的心肌细胞损伤。在 ISO 下转染 miR-18a-5p 降低了 1% ISO 对心肌细胞损伤的保护作用。荧光素酶报告基因检测证实CCND2可能是miR-18a-5p的靶基因。在心肌体外细胞模型中，ISO通过下调miR-18a-5p的表达来减轻缺氧/复氧引起的心肌细胞损伤。