| 杨永秀,赵锋.维生素 D受体对心肌缺血再灌注损伤的影响及作用机制[J].安徽医药,2021,25(4):773-777. |
| 维生素 D受体对心肌缺血再灌注损伤的影响及作用机制 |
| Effect of vitamin D receptor (VDR) on myocardial ischemia-reperfusion injury and its mechanism |
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| DOI：10.3969/j.issn.1009-6469.2021.04.034 |
| 中文关键词: 受体，骨化三醇 心肌再灌注损伤 血流动力学 心肌梗死面积 心功能 |
| 英文关键词: Receptors, calcitriol Myocardial reperfusion injury Hemodynamics Myocardial infarct size Cardiac function |
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| 中文摘要: |
| 目的探讨维生素 D受体(vitamin D receptor，VDR)对心肌缺血再灌注损伤的影响及作用机制。方法 2018年 12月至 2019年 1月，选择野生型雄性 C57BL/6小鼠 60只作为研究对象，构建小鼠心肌缺血再灌注损伤模型，并将小鼠按照随机数字表法进行分组，分为假手术组、 Vehicle组、 Calcitriol组和 PC组，每组 15只，对 Vehicle组给予腹腔注射 Vehicle，给予 Calcitriol组腹腔注射 Calcitriol，给予 PC组腹腔注射 PC，按照缺血 30 min+再灌注 24 h的方法进行研究，在再灌注 24 h后，对小鼠血流动力学、心肌梗死面积和心功能指标进行测定。结果各组小鼠缺血相关范围差异无统计学意义， Calcitriol组(23.11±3.41)%和 PC组(26.72±2.67)%小鼠的心肌梗死面积明显小于对照组(44.22±3.12)%，经检验，均 P<0.05，与假手术组相比，再灌注 24 h后的 Vehicle组小鼠的心肌摄取 18F-FDG的标准摄取值(SUV)显著降低， Calcitriol组和 PC组中小鼠心肌摄取 18F-FDG的 SUV值明显较 Vehicle组高(P<0.000 1)Calcitriol组和 PC组的左心室射血分数(LVEF)和缩短分数(LVFS)显著高于 Vehicle组(P<0.000 1)。在观察缺血再灌注的中激活 VDR对小鼠心肌缺血再灌注后的血流动力学差异无统计学意义。结论通过药过程，理学方法激活 VDR能够有效减轻心肌缺血再灌注损伤，可以作为治疗缺血性心脏病的新的干预靶点进行深入探讨。 |
| 英文摘要: |
| Objective To investigate the effect of vitamin D receptor (VDR) on myocardial ischemia-reperfusion injury and its mechanism.Methods During December 2018-January 2019 sixty wild-type male C57BL/6 mice were selected as the research objects to construct a mouse myocardial ischemia-reperfusion injury model, and the mice were grouped according to the random number tablemethod and assigned into sham operation group, Vehicle group, Calcitriol group and PC group, 15 mice in each group. Vehicle groupwas given intraperitoneal injection of Vehicle, Calcitriol group was given intraperitoneal injection of Calcitriol, and PC group was givenintraperitoneal injection of PC. The study was carried out according to the method of 30 minutes of ischemia + 24 hours of reperfusion.Later, the hemodynamics, myocardial infarction area and cardiac function indexes of mice were measured.Results There was no significant difference in the range of ischemia in each group of mice. The area of myocardial infarction in Calcitriol group (23.11±3.41)%and PC group (26.72±2.67)% was significantly smaller than that of control group (44.22±3.12)% (all P<0.05). Compared with sham operation group, the standard uptake value (SUV) of 18F-FDG uptake in the myocardium of mice in Vehicle group after 24 h reperfusionwas significantly lowered, while that of the mice was significantly higher in Calcitriol group and PC group than in Vehicle group (P<0.000 1). The left ventricular ejection fraction (LVEF) and fractional shortening (LVFS) of Calcitriol group and PC group were significantly higher than those of Vehicle group (both P<0.000 1). In the process of ischemia-reperfusion observation, activation of VDR had no significant difference in hemodynamics after myocardial ischemia-reperfusion in mice.Conclusion VDR activation through pharmacological methods can effectively reduce myocardial ischemia-reperfusion injury, and can be used as a new intervention target for the treatment of ischemic heart disease for in-depth discussion. |
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