| 心肌脂联素信号通路增强可能是心肌缺血预处理保护心肌的部分新机制 |
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| 引用本文： | 宋延彬,张君毅,张云清.心肌脂联素信号通路增强可能是心肌缺血预处理保护心肌的部分新机制[J].心脏杂志,2017,29(1):29-33. |
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| 作者姓名： | 宋延彬 张君毅 张云清 |
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| 作者单位： | （延安大学附属医院:1.心内科，2.产科，陕西 延安 716000，3.空军工程大学门诊部，陕西 西安 713800，4.第四军医大学西京医院心内科，陕西 西安 710032） |
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| 基金项目： | 延安医疗卫生攻关计划项目资助（2015KW-04）
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| 摘 要： | 目的 探讨脂联素(APN)信号通路在心肌缺血预处理中的作用及机制。方法 建立对照组，心肌缺血预处理(ischemic preconditioning,IPC)和缺血/再灌注(myocardial ischemia/reperfusion，MI/R)损伤小鼠模型，每组8只C57BL/6J小鼠。ELISA法检测血浆APN水平，超声检测心功能，TTC法观察心肌梗死面积，TUNEL染色检测心肌细胞凋亡，Western blot检测APN受体（adiponectin receptor，AdipoR）, 腺苷酸活化蛋白激酶(adenosine monophosphate activated protein kinase,AMPK)分子的表达。结果 与对照组血浆APN〔(19.08±2.15)μg/ml〕相比，IPC组和MI/R组缺血30 min后血浆APN水平降低（P<0.01）；与IPC组血浆APN〔(15.4±2.09)μg/ml〕相比，MI/R组血浆APN水平降至更低〔(13.95±1.75)μg/ml〕（P<0.05）；与对照组左室射血分数(76.37±7.24)相比，MI/R组和IPC组左室射血分数（57.15±7.32和66.37±6.09）均降低（P<0.05）；与MI/R组左室射血分数相比，IPC组左室射血分数升高（P<0.01）；与对照组左室短轴缩短率(52.13±4.80)相比，MI/R组和IPC组左室短轴缩短率（37±8.14和44.9±6.52）降低（P<0.01）；与MI/R组左室短轴缩短率相比，IPC组左室短轴缩短率升高（P<0.01）；与对照组左室舒张末内径〔(3.13±0.59)mm〕相比，MI/R组和IPC组左室舒张末内径增加〔(3.50±0.48)mm和(3.23±0.50)mm〕（P<0.05）；与MI/R组左室左室舒张末内径相比，IPC组左室舒张末内径减少（P<0.01）；与对照组左室收缩末内径（1.95±0.59）mm相比，MI/R组和IPC组左室左室收缩末内径增加分别为〔(2.26±0.48)mm和(2.15±0.21)mm〕（P<0.05）；与MI/R组左室左室收缩末内径相比，IPC组左室收缩末内径减少（P<0.01）；与对照组心肌梗死面积相比，MI/R组和IPC组心肌梗死面积增加（45.7±3.92，40.9±4.1）（P<0.01）；与MI/R组心肌梗死面积相比，IPC组心肌梗死面积增加减少（P<0.05）；与对照组TUNEL阳性细胞相比，MI/R组和IPC组TUNEL阳性细胞增加（12.16±1.93和8.96±1.49）（P<0.01）；与MI/R组TUNEL阳性细胞相比，IPC组TUNEL阳性细胞减少（P<0.05）；与对照组Caspase-3活力〔(1.93±1.82)nmol/(h·mg)〕相比，MI/R组和IPC组Caspase-3活力增加〔(5.82±2.72和4.68±2.31）nmol/（h·mg）〕（P<0.01）；与MI/R组Caspase-3活力相比，IPC组Caspase-3活力减少（P<0.05）；与对照组心肌AdipoR1的表达(0.86±0.26)相比，MI/R组和IPC组心肌AdipoR1表达减少（0.57±0.15和0.72±0.22）（P<0.05）；与MI/R组心肌AdipoR1的表达相比，IPC组心肌AdipoR1的表达增加（P<0.05）；而AdipoR2的表达没有变化；与对照组心肌pAMPK/AMPK的表达(1.6±0.24)相比，MI/R组和IPC组心肌pAMPK/AMPK的表达减少（1.04±0.13和1.28±0.13）（P<0.05）；与MI/R组心肌pAMPK/AMPK的表达相比，IPC组心肌pAMPK/AMPK的表达增加（P<0.01）。结论 缺血预处理减轻心肌再灌注损伤机制部分可能在于心肌APN/AdipoR/AMPK信号通路增强。
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| 关 键 词： | 缺血预处理 缺血/再灌注损伤 心肌 脂联素 脂联素受体 |
| 收稿时间： | 2015-07-21 |
Decreased myocardial ischemia/reperfusion injury in ischemic preconditioning may in part involve cardiac adiponectin signal sufficiency |
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| Abstract: | AIM To delineate the role of adiponectin (APN) signal pathway in ischemic preconditioning (IPC) and the underlying mechanisms. METHODSWe induced IPC and myocardial ischemia/reperfusion (MI/R) model with eight C57BL/6J mice in each group by the classical method. APN content was determined by ELISA, cardiac function was determined by noninvasive echocardiography and MI size was determined by Evans blue/TTC double staining method. Myocardial apoptosis was determined within the entire I/R region via TUNEL staining and caspase-3 activity assay and adiponectin receptor (AdipoR)/AMPK expression was determined by Western blot. RESULTSCompared with control group, APN level (19.08±2.15) μg/ml in plasma, MI/R and IPC group APN level in plasma declined (P<0.01). Compared with IPC group, APN level (15.4±2.09) μg/ml, MI/R group APN level (13.95±1.75) μg/ml was markedly decreased (P<0.05). Compared with control group, left ventricular ejection fraction (LVEF) (76.37±7.24), MI/R and IPC group LVEF were all decreased (P<0.01). Compared with IPC group LVEF (66.37±6.09), MI/R group LVEF (57.15±7.32) was markedly decreased (P<0.01). Compared with control group, left ventricular fraction shortening (LVFS) (52.13±4.80), MI/R and IPC group LVFS were all decreased (P<0.05). Compared with IPC group, LVFS (44.9±6.52), MI/R group LVFS (37±8.14) was markedly decreased (P<0.01). Compared with control group, left ventricular internal diameters of diastole (LVIDd) (3.13±0.59) mm, MI/R and IPC group LVIDd were all increased (P<0.05). Compared with IPC group LVIDd (3.23±0.50 mm), MI/R group LVIDd (3.50±0.48) mm was markedly increased (P<0.01). Compared with control group, left ventricular internal diameters of diastole (LVIDds) (1.95±0.59) mm, MI/R and IPC group LVIDds were all increased (P<0.05). Compared with IPC group LVIDds (2.15±0.21) mm, MI/R group LVIDd (2.26±0.48) mm was markedly increased (P<0.05). Compared with control group, myocardial infarct size, MI/R and IPC group myocardial infarct size were all increased (P<0.01). Compared with IPC group, myocardial infarct size (40.9±4.1), MI/R group myocardial infarct size (45.7±3.92) was markedly increased (P<0.05). Compared with control group TUNEL staining, MI/R and IPC group TUNEL staining were all increased (P<0.01). Compared with IPC group TUNEL staining (8.96 ± 1.49), MI/R group TUNEL staining (12.16±1.93) was markedly increased (P<0.05) Compared with control group, caspase-3 activity (1.93±1.82) nmol/(h·mg), MI/R and IPC group caspase-3 activity were all increased (P<0.01). Compared with IPC group caspase-3 activity (4.68±2.31) nmol/(h·mg), MI/R group caspase-3 activity (5.82±2.72) nmol/(h·mg) was markedly increased (P<0.05). Compared with control group, AdipoR1 expression (0.86±0.26), MI/R and IPC group AdipoR1 expression were all decreased (P<0.01). Compared with IPC group, AdipoR1 expression (0.72±0.22), MI/R group AdipoR1 expression (0.57±0.15) was markedly decreased (P<0.05). However, AdipoR2 expression showed no significant change. Compared with control group, pAMPK/AMPK expression (1.6±0.24), pAMPK/AMPK expression were all decreased (P<0.05). Compared with IPC group, pAMPK/AMPK expression (1.28±0.13), MI/R group AdipoR1 expression (1.04±0.13) was markedly decreased (P<0.05). CONCLUSIONDecreased myocardial ischemia/reperfusion injury in IPC may involve cardiac adiponectin signal sufficiency in part and presents the best opportunity to improve outcomes for patients after acute coronary syndrome by increasing the cardiac adiponectin signal. |
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