| 杨华,康雅琴,李娟.七氟醚调控HIF1信号通路对糖尿病大鼠心肌IR损伤的保护作用.[J].中南医学科学杂志.,2025,(2):236-240. |
| 七氟醚调控HIF1信号通路对糖尿病大鼠心肌IR损伤的保护作用 |
| Protective effects of sevoflurane on myocardial ischemia-reperfusion injury in diabetic rats by regulating HIF-1 signaling pathway |
| 投稿时间：2024-05-06 修订日期：2024-12-10 |
| DOI：10.15972/j.cnki.43-1509/r.2025.02.010 |
| 中文关键词: 低氧诱导因子-1 糖尿病 大鼠 七氟醚 心肌缺血再灌注 线粒体自噬 [ |
| 英文关键词:HIF-1 diabetes rats sevoflurane myocardial ischemia reperfusion mitophagy |
| 基金项目:荆州市科技计划项目(20230193) |
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| 中文摘要: |
| 目的探讨七氟醚调控低氧诱导因子-1(HIF-1)信号通路对糖尿病大鼠心肌缺血再灌注(IR)损伤的保护作用。 方法选择雄性糖尿病大鼠分为假手术组、模型组、七氟醚组、2ME2组(HIF-1抑制剂)、2ME2+七氟醚组。除假手术组外,其他4组均制备糖尿病心肌IR损伤模型。检测各组大鼠心脏功能、心肌梗死面积、自噬小体数量,以及心肌组织HIF-1α、BNIP3、LC3BII/LC3BI、Beclin-1表达水平。 结果与假手术组相比,其他4组心肌梗死面积、自噬小体数量升高,且七氟醚组低于模型组,2ME2组、2ME2+七氟醚组高于七氟醚组(P＜0.05)。与假手术组相比,其他4组左室射血分数、短轴缩短率降低,七氟醚组高于模型组,2ME2组、2ME2+七氟醚组低于七氟醚组(P＜0.05)。与假手术组相比,其他4组HIF-1α、BNI3P、LC3BII/LC3BI、Beclin-1蛋白表达均升高(P＜0.05)。七氟醚组HIF-1α、BNI3P蛋白高于模型组,LC3BII/LC3BI、Beclin-1蛋白低于模型组；2ME2组、2ME2+七氟醚组HIF-1α、BNI3P低于七氟醚组,LC3BII/LC3BI、Beclin-1蛋白高于七氟醚组(P＜0.05)。 结论七氟醚通过上调HIF-1信号通路来改善糖尿病大鼠心肌缺血再灌注损伤。 |
| 英文摘要: |
| AimTo investigate the protective effects of sevoflurane on myocardial ischemia-reperfusion (IR) injury in diabetic rats by regulating HIF-1 signaling pathway. MethodsMale diabetic rats were divided into sham operation group, model group, sevoflurane group, 2ME2 group (HIF-1 inhibitor), and 2ME2+sevoflurane group. Except the sham operation group, the other four groups were used to establish diabetic myocardial IR injury models. Cardiac function, myocardial infarction area, autophagosome number, and the expression levels of HIF-1α, BNIP3, LC3BII/LC3BI, and Beclin-1 in myocardial tissue were measured. ResultsCompared with the sham operation group, the myocardial infarction area and autophagosome number in the other four groups were increased, and the sevoflurane group was lower than the model group, while the 2ME2 group and 2ME2+sevoflurane group were higher than the sevoflurane group (P＜0.05). Compared with the sham operation group, left ventricular ejection fraction and fractional shortening in the other four groups were decreased, and the sevoflurane group was higher than the model group, while the 2ME2 group and 2ME2+sevoflurane group were lower than the sevoflurane group (P＜0.05). Compared with the sham operation group, the expression levels of HIF-1α, BNIP3, LC3BII/LC3BI, and Beclin-1 proteins in the other four groups were increased (P＜0.05). The sevoflurane group had higher HIF-1α and BNIP3 protein levels than the model group, while LC3BII/LC3BI and Beclin-1 protein levels were lower than the model group. The 2ME2 group and 2ME2+sevoflurane group had lower HIF-1α and BNIP3 protein levels than the sevoflurane group, while LC3BII/LC3BI and Beclin-1 protein levels were higher than the sevoflurane group (P＜0.05). ConclusionSevoflurane improves myocardial IR injury in diabetic rats by upregulating the HIF-1 signaling pathway. |
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