| 摘要: |
| 目的：研究高脂饲喂ApoE-/-小鼠的动脉粥样硬化小鼠心肌缺血再灌注模型。方法：将28只ApoE-/-小鼠按体质量随机分为2组：正常对照组（10只）、模型组（18只）。正常对照组常规饲养，模型组给予高脂饲料16周建立动脉粥样硬化模型。造模成功后，将模型组16只随机分为2组：模型对照组、乙醇损伤组，每组各8只。模型对照组继续进行高脂造模，乙醇损伤组在给予高脂饲料的同时日常饮用25%的乙醇10μl，正常对照组给予普通饲料饲养。连续4周。造模结束后，采用离体灌流装置（Langendorff）对各组心脏进行离体灌流，并对模型对照组小鼠离体心脏进行冠状动脉左前降支结扎，结扎30 min，复灌120 min。检测灌流复灌5 min和10 min时灌流液中乳酸脱氢酶（LDH）的含量，心肌组织中半胱氨酸蛋白酶-3(Caspase-3)和乙醛脱氢酶2(ALDH2)的含量。测定心肌梗死面积，并对心肌组织进行组织病理学检查。结果：模型组小鼠主动脉脂质斑块形成，血管壁可见内膜明显增厚，血管狭窄；缺血再灌注模型ApoE-/-小鼠在结扎LAD前心电图ST段抬高，提示造模成功。小鼠心脏复灌5 min和10 min灌流液中LDH含量及心肌组织中Caspase-3、ALDH2含量，心肌梗死面积，心肌组织病理评分方面，模型对照组、乙醇损伤组与正常对照组比较，乙醇损伤组与模型对照组比较，差异均有统计学意义（P<005或P<001）。ApoE-/-小鼠心肌组织TTC染色结果显示，与正常对照组比较，模型对照组心肌梗死部位明显增加，与模型对照组比较，乙醇损伤组心肌梗死面积明显减少。结论：乙醇诱导对ApoE-/-动脉粥样硬化小鼠心肌缺血再灌注具有明显的保护作用，其机制与调节Caspase-3、ALDH2含量有关。 |
| 关键词: 心肌缺血再灌注 ApoE-/-小鼠 Caspase-3 ALDH2 实验研究 |
| DOI： |
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| Intervention effect of alcohol on an ApoE-/- mouse model of ex vivo myocardial ischemia/reperfusion：An experimental study |
| LIN Xinwen,CHEN Na,CHEN Wenming |
| (Hunan Drug Inspection Center，Changsha 410001，Hunan，China;The First Affiliated Hospital of Hunan University of Chinese Medicine，Changsha 410007，Hunan，China) |
| Abstract: |
| Objective：To establish an ApoE-/- mouse model ofatherosclerosis and myocardial ischemia/reperfusion by feeding high-fat dietMethods：A total of 28 ApoE-/- mice were divided into normal control group with 10 mice and model group with 18 mice based on body weightThe mice in the normal control group were given routine feeding，and those in the model group were given high-fat diet for 16 weeks to establish a model of atherosclerosisAfter successful modeling，the 16 mice in the model group were further divided into model control group and alcohol injury group，with 8 mice in each groupThe mice in the model control group were given high-fat diet，those in the alcohol injury group were given high-fat diet and 10μL 25% alcohol，and those in the normal control group were given normal diet，for 4 consecutive weeksAfter modeling，Langendorff perfusion device was used to perform ex vivo heart perfusion，and ligation of the left anterior descending coronary artery (LAD) was performed for the isolated hearts of the mice in the model control group for 30 minutes，followed by reperfusion for 120 minutesThe content of lactate dehydrogenase (LDH) in perfusion fluid and the content of caspase-3 and aldehyde dehydrogenase 2(ALDH2) in myocardial tissue were measured at 5 and 10 minutes of reperfusionMyocardial infarct area was measured，and histopathological examination was performed for myocardial tissueResults：The mice in the model group had the formation of lipid plaques in the aorta，significant intimal thickening，and vascular stenosis，and the ApoE-/- mice with ischemia/reperfusion had ST-segment elevation before LAD ligation，suggesting that the model was successfully establishedThere were significant differences in the content of LDH in perfusion fluid and the content of caspase-3 and ALDH2 in myocardial tissue at 5 and 10 minutes of reperfusion，myocardial infarct area，and pathological score of myocardial tissue between the model control group and the normal control group，between the alcohol injury group and the normal control group，and between the alcohol injury group and the model control group (P＜005 or P＜001)TTC staining of the myocardial tissue of ApoE-/- mice showed that compared with the normal control group，the model control group had a significant increase in myocardial infarct area，and compared with the model control group，the alcohol injury group had a significant reduce in myocardial infarct areaConclusion：Alcohol induction has a marked protective effect against myocardial ischemia/reperfusion in ApoE-/- mice with atherosclerosis，possibly by regulating the content of caspase-3 and ALDH2 |
| Key words: myocardial ischemia/reperfusion ApoE-/- mouse caspase-3 aldehyde dehydrogenase 2 experimental study |
