| 王洋洋,杨英来,信小兵,陈嘉媛,韩媛媛,李丽丹,朱丽丽,陈浣洁,邹 燕,雷 琎,李婷婷,耿广耀,王新春.刺槐素对大鼠心肌缺血再灌注损伤的保护作用与机制研究[J].,2022,(24):4639-4643 |
| 刺槐素对大鼠心肌缺血再灌注损伤的保护作用与机制研究 |
| Protective Effect and Mechanism of Acacetin on Myocardial Ischemia Reperfusion Injury in Rats |
| 投稿时间：2022-05-06 修订日期：2022-05-31 |
| DOI：10.13241/j.cnki.pmb.2022.24.007 |
| 中文关键词: 刺槐素 心肌缺血再灌注损伤 Jak2/Stat3信号通路 凋亡 |
| 英文关键词: Acacetin Myocardial ischemia reperfusion injury Jak2/Stat3 Apoptosis |
| 基金项目:国家自然科学基金项目（81860747；81960766）；国家大学生创新训练计划项目（202013560003） |
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| 中文摘要: |
| 摘要 目的：探讨刺槐素对大鼠心肌缺血再灌注损伤(MIRI)的作用以及可能的作用机制。方法：对24只Sprague-Dawley (SD)大鼠进行随机分组，分为：假手术组、模型组、刺槐素给药组、刺槐素+AG490给药组，每组6只，通过结扎冠状动脉左前降支，缺血30 min，再灌注120 min复制心肌缺血再灌注损伤模型。利用氯化三苯基四氮唑测定心肌梗死面积，紫外分光光度计和酶联免疫法检测血清中肌酸激酶同工酶（CK-MB）、乳酸脱氢酶（LDH）的活性，蛋白印迹法分别检测心肌组织中Bcl-2、Bax、Stat3和p-Stat3蛋白相对表达水平。结果：与假手术组比较，模型组大鼠血清中CK-MB、LDH活性明显升高（P＜0.01），心肌梗死面积百分比显著增加（P＜0.01），p-Stat3/Stat3比率、Bcl-2/Bax比率显著下降（P＜0.01）；与模型组相比，刺槐素给药组中CK-MB、LDH的活性，以及心肌梗死面积百分比显著降低（P＜0.01），Bcl-2/Bax比率和p-Stat3/Stat3比率显著提高（P＜0.05）。然而在刺槐素+AG490药物组中刺槐素对于受损心肌的保护作用被AG490消除。结论：刺槐素可减轻MIRI大鼠心肌损伤，发挥心肌保护作用，其机制可能与活化Jak2/Stat3信号通路进而抑制心肌细胞凋亡有关。 |
| 英文摘要: |
| ABSTRACT Objective: To explore the effect of acacetin on myocardial ischemia reperfusion injury in rats and its possible mechanism. Methods: 24 SPF rats were randomly divided into sham operation group, model control group, acacetin administration group, acacetin+AG490 group, with 6 rats in each group. Myocardial ischemia reperfusion injury model was induced by 30 minutes coronary occlusion followed by 2 h reperfusion in rats. The myocardial infarct area was measured by triphenyltetrazolium chloride, the activities of CK-MB and LDH in serum were detected by ultraviolet spectrophotometer and enzyme linked immunoassay, and the relative expression levels of Bcl-2, Bax, Stat3 and p-Stat3 proteins in myocardium were investigated by Western blot. Results: Compared with the sham operation group, the activities of CK-MB and LDH in serum rose obviously in the model group (P<0.01), the percentage of myocardial infarction area increased significantly (P<0.01), the ratio of p-Stat3/Stat3 and Bcl-2/Bax decreased notably (P<0.01); Compared with the model group, the activities of CK-MB and LDH, the percentage of myocardial infarction area were significantly decreased (P<0.05), and the ratios of Bcl-2/Bax and p-Stat3/Stat3 were increased significantly in the acacetin treated group. However, the protective effect of acacetin on damaged myocardium was cleared by AG490 in the group of acacetin+AG490. Conclusion: Acacetin could alleviate myocardial damage and exert myocardial protection in MIRI rats, and its mechanism might be related to the inhibition of cardiomyocyte apoptosis by activating Jak2/Stat3 signal pathway. |
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