间歇有氧运动训练改善肥胖小鼠缺血后心脏功能恢复被引量：5

Aerobic interval training improves cardiac function recovery after ischemia in obese mice

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摘要目的探讨有氧间歇运动训练(AIT)对高脂饮食诱导的肥胖小鼠心肌缺血再灌注(MI/R)损伤的影响和相关机制。方法 30只2月龄C57小鼠随机分为:正常对照组;高脂饮食组;高脂饮食间歇训练组。喂养12周后,建立急性MI/R模型(缺血30 min,再灌注4 h)。于再灌注结束后不同时间点采用超声心动仪检测心脏功能,Western blot法检测心脏相关信号表达。结果与正常对照组相比,12周高脂饮食喂养导致小鼠肥胖,体质量显著增加(P<0.05);AIT可有效降低高脂饮食肥胖小鼠的体质量,增加心脏质量/胫骨长度比率(P<0.05);与正常对照组相比,高脂饮食肥胖小鼠MI/R损伤显著加重(P<0.05);AIT可有效减轻肥胖小鼠心肌损伤,减小心肌梗死面积和血清LDH水平(均P<0.05);AIT还显著改善MI/R后心肌功能恢复,有效提高左室射血分数(EF)和左室短轴缩短率(FS)(均P<0.05)。与高脂饮食组相比,AIT可显著增强高脂饮食肥胖小鼠心肌线粒体SIRT3和MnSOD表达,减少高脂饮食组MI/R心肌组织氧化应激(均P<0.05)。结论 AIT可有效提高高脂饮食肥胖小鼠心肌线粒体SIRT3和MnSOD表达,增加线粒体抗氧化酶活性,进而减轻肥胖小鼠的MI/R损伤,促进缺血后心脏功能恢复。 AIM To evaluate the effect of aerobic interval training （AIT） on myocardial ischemia reper- fusion （MI/R） injury in high-fat diet-induced obese mice and the related mechanism. METHODS Sixty 2-month-old C57 mice were randomly divided into three groups： control mice with normal diet （Con）, high-fat diet （HF） and high-fat diet mice with AIT （HF ＋ AIT）. Twelve weeks after feeding mice were subjected to acute myocardial ischemia reperfusion （ ischemia 30 min/reperfusion 4 h）. Cardiac function was determined by echocardiography and related signal protein expression was detected by Western blot. RESULTS Twelve-week high-fat feeding led to obesity in mice and their weight significantly increased compared to control mice. AIT training effectively reduced the weight of HF mice and increased heart weight/tibia length ratio. Compared with control group, MI/R injury in HF obese mice significantlyincreased. AIT training effectively reduced MI/R injury in HF mice as evidenced by reduced infarct area and serum LDH level （P 〈 0. 05）. AIT training also significantly improved myocardial functional recovery after MI/R, effectively improved left ventricular ejection fraction （EF） and decreased left ventricular short axis ratio （FS）. Compared with HF group, AIT significantly enhanced the myocardial mitochondria SIRT3 and MnSOD expression in HF mice and reduced MI/R myocardial tissue oxidative stress in HF mice （P 〈 0. 05 ）. CONCLUSION AIT effectively improves myocardial mitochondria SIRT3 and MnSOD in HF obese mice and increases mitochondrial antioxidant enzyme activity, thus reducing the obese mice MI/R injury and promoting heart function recovery after ischemia.