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Combined administration of lauric acid and glucose improved cancer‐derived cardiac atrophy in a mouse cachexia model

机译:月桂酸和葡萄糖的组合给药改善了小鼠肠病模型中的癌症衍生的心脏萎缩

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摘要

Cancer‐derived myocardial damage is an important cause of death in cancer patients. However, the development of dietary interventions for treating such damage has not been advanced. Here, we investigated the effect of dietary intervention with lauric acid (LAA) and glucose, which was effective against skeletal muscle sarcopenia in a mouse cachexia model, on myocardial damage. Treatment of H9c2 rat cardiomyoblasts with lauric acid promoted mitochondrial respiration and increased ATP production by Seahorse flux analysis, but did not increase oxidative stress. Glycolysis was also promoted by LAA. In contrast, mitochondrial respiration and ATP production were suppressed, and oxidative stress was increased in an in vitro cachexia model in which cardiomyoblasts were treated with mouse cachexia ascites. Ascites‐treated H9c2 cells with concurrent treatment with LAA and high glucose showed that mitochondrial respiration and glycolysis were promoted more than that of the control, and ATP was restored to the level of the control. Oxidative stress was also reduced by the combined treatment. In the mouse cachexia model, myocardiac atrophy and decreased levels of a marker of muscle maturity, SDS‐soluble MYL1, were observed. When LAA in CE‐2 diet was orally administered alone, no significant rescue was observed in the cancer‐derived myocardial disorder. In contrast, combined oral administration of LAA and glucose recovered myocardial atrophy and MYL1 to levels observed in the control without increase in the cancer weight. Therefore, it is suggested that dietary intervention using a combination of LAA and glucose for cancer cachexia might improve cancer‐derived myocardial damage.
机译:癌症源性心肌损伤是癌症患者死亡的重要原因。但是,粮食干预措施的发展尚未进入。在这里,我们研究了膳食干预与月桂酸(LAA)和葡萄糖的影响,这对于小鼠粪便模型中的骨骼肌Sarcopenia有效,对心肌损伤有效。用桂酸治疗H9C2大鼠心肌细胞促进线粒体呼吸的促进线粒体呼吸和升高的ATP产量增加,但未增加氧化应激。 Laa还促进了糖酵解。相比之下,抑制了线粒体呼吸和ATP产量,并且在体外恶毒酶模型中增加了氧化应激,其中用小鼠肠道腹水处理心肌细胞。腹水处理的H9C2细胞与LAA和高葡萄糖的同时处理显示,促进了比对照的大多数线粒体呼吸和糖醇,并且ATP恢复到对照的水平。结合治疗也降低了氧化应激。在小鼠的恶作剧模型中,观察到肌肉成熟,SDS可溶性myL1的肌肉成熟度标记的心肌萎缩和降低。当单独口服Laa在CE-2饮食中,在癌症衍生的心肌病症中没有观察到显着的救援。相比之下,Laa和葡萄糖的组合口服给予在控制中观察到的心肌萎缩和MyL1至水平,而不会增加癌症重量。因此,建议使用LAA和葡萄糖组合的膳食干预用于癌症恶病症可能改善癌症源性心肌损伤。

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