血管内皮生长因子受体-1的表达上调参与七氟醚预处理介导的心肌保护作用
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Upregulation of vascular endothelial growth factor receptor-1 contributes to sevoflurane preconditioning-mediated cardioprotection
背景与目的：七氟醚预处理（SPC）产生的心肌保护作用类似于缺血预处理，但SPC的具体机制尚不清楚。有研究表明血管内皮生长因子受体-1（VEGFR-1）参与缺血预处理介导的心脏保护作用。本研究旨在探讨VEGFR-1在SPC介导的心脏保护作用中的重要性。
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方法：七氟醚预处理（SPC）产生的心肌保护作用类似于缺血预处理，但SPC的具体机制尚不清楚。有研究表明血管内皮生长因子受体-1（VEGFR-1）参与缺血预处理介导的心脏保护作用。本研究旨在探讨VEGFR-1在SPC介导的心脏保护作用中的重要性。
结果：与I/R组相比，2.5％七氟醚预处理可显著改善心功能，减少心肌梗塞面积，减少心肌酶释放，上调VEGFR-1表达，并减轻炎症反应。此外，选择性VEGFR-1激动剂（胎盘生长因子）不能增强七氟醚的心脏保护和抗炎作用，而特异性VEGFR-1抑制剂（MF1）完全逆转这些作用。
结论：2.5％七氟醚预处理可减轻心肌I/R损伤，这可能与抗炎特性和VEGFR-1的表达上调有关。
Bin Qian，Yang Yang，Yusheng Yao，Yanlin Liao，Ying Lin； Upregulation of vascular endothelial growth factor receptor-1 contributes to sevoflurane preconditioning-mediated cardioprotection；Drug Design, Development and Therapy 2018:12 769–776
BACKGROUND: Sevoflurane preconditioning (SPC) can provide myocardial protective effects similar to ischemic preconditioning. However, the exact mechanism of SPC remains unclear. Previous studies indicate that vascular endothelial growth factor receptor-1 (VEGFR-1) is involved in ischemic preconditioning-mediated cardioprotection. This study was designed to determine the significance of VEGFR-1 signaling in SPC-mediated cardioprotection.
METHODS:Myocardial ischemia–reperfusion (I/R) rat model was established using the Langendorff isolated heart perfusion apparatus. Additionally, after 15 min of baseline equilibration, the isolated hearts were pretreated with 2.5% sevoflurane, 2.5% sevoflurane+MF1 10 μmol/L, or 2.5% sevoflurane+placental growth factor 10 μmol/L, and then subjected to 30 min of global ischemia and 120 min of reperfusion. The changes in hemodynamic parameters, myocardial infarct size, and the levels of creatine kinase-MB, lactate dehydrogenase, cardiac troponin-I, tumor necrosis factor-α, and interleukin 6 in the myocardium were evaluated.
RESULTS:Compared to the I/R group, pretreatment with 2.5% sevoflurane significantly improved the cardiac function, limited myocardial infarct size, reduced cardiac enzyme release, upregulated VEGFR-1 expression, and decreased inflammation. In addition, the selective VEGFR-1 agonist, placental growth factor, did not enhance the cardioprotection and anti-inflammation effects of sevoflurane, while the specific VEGFR-1 inhibitor, MF1, completely reversed these effects.
CONCLUSIONS:Our data have demonstrated that 2.5% sevoflurane preconditioning alleviates heart I/R injury, which is probably mediated by the anti-inflammatory property and upregulation of VEGFR-1.
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