One of the common negative impacts in the management of acute myocardial infarction is cognitive decline. Using the rat model of isoproterenol (ISO)‐induced myocardial infarction, we assessed the cardioprotective effect of sodium thiosulfate (STS) and its influence on cognition. STS treatment reduced the cardiac infarct size by 75%, injury markers (lactate dehydrogenase: 60%, creatine kinase‐muscle/brain: 44%) release in the blood, maintain the heart rate within a normal range (365 ± 10 bpm) and minimize postinfarction hypertrophic changes in comparison with the ISO group. At the cellular level, the heart from these rats had reduced reactive oxygen species (ROS) (25%), caspase‐9 (60%), and improved mitochondrial function (restored electron transport chain function and copy number) compared to ISO hearts. The brain of STS‐treated rats also showed a reduction in ROS (45%), caspase‐9 (37%), and improved mitochondrial function relative to the brain of the ISO group, particularly limited to the striatum region, and these rats showed improved cognitive ability. Predominantly, the STS treatment reduced the reference memory defects observed in comparison to rats challenged by ISO. Furthermore, elevated circulating mitochondrial DNA and ATP were found in ISO‐challenged rats, which indicate the cardiac mitochondria linked damage‐associated patterns were restored to the sham level when pretreated with STS. We found increased H₂S, a well‐known metabolite of STS with a neuroprotective role in the brain after STS administration, hinting at a possible secondary defense mechanism. In conclusion, the STS mediated cardioprotection and its nootropic effects are primarily mediated via the improvement of mitochondrial function and reduction of oxidative stress.

中文翻译：

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在梗死异丙肾上腺素模型中，硫代硫酸钠的有益作用超出了心肌组织：对促智作用的意义。

在急性心肌梗死的管理中常见的负面影响之一是认知能力下降。使用异丙肾上腺素（ISO）诱发的大鼠心肌梗死模型，我们评估了硫代硫酸钠（STS）的心脏保护作用及其对认知的影响。STS治疗使心脏梗死面积减少了75％，损伤标志物（乳酸脱氢酶：60％，肌酸激酶-肌肉/大脑：44％）释放到血液中，将心率维持在正常范围内（365±10 bpm），并且与ISO组相比，将梗死后肥厚性变化降至最低。在细胞水平上，与ISO心脏相比，这些大鼠的心脏减少了活性氧（ROS）（25％），半胱天冬酶9（60％）并改善了线粒体功能（恢复了电子传输链功能和拷贝数）。与ISO组相比，经STS处理的大鼠的大脑还表现出ROS降低（45％），caspase-9（37％）并改善了线粒体功能，特别是局限于纹状体区域。提高认知能力。与接受ISO攻击的大鼠相比，STS治疗主要减少了观察到的参考记忆缺陷。此外，在受ISO挑战的大鼠中发现循环线粒体DNA和ATP升高，这表明用STS预处理后，与心脏线粒体相关的损伤相关模式已恢复到假水平。我们发现H增加 与通过ISO挑战的大鼠相比，STS处理减少了观察到的参考记忆缺陷。此外，在受ISO挑战的大鼠中发现循环线粒体DNA和ATP升高，这表明用STS预处理后，与心脏线粒体相关的损伤相关模式已恢复到假水平。我们发现H增加 与通过ISO挑战的大鼠相比，STS处理减少了观察到的参考记忆缺陷。此外，在受ISO挑战的大鼠中发现循环线粒体DNA和ATP升高，这表明用STS预处理后，与心脏线粒体相关的损伤相关模式已恢复到假水平。我们发现H增加₂ S，一种众所周知的STS代谢产物，在STS给药后对大脑具有神经保护作用，提示可能存在次级防御机制。总之，STS介导的心脏保护作用及其促智作用主要是通过改善线粒体功能和减少氧化应激来介导的。