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Research Article

N-乙酰半胱氨酸减轻慢性肝病引起的肌肉减少和肌肉凋亡

卷 20, 期 1, 2020

页: [60 - 71] 页: 12

弟呕挨: 10.2174/1566524019666190917124636

价格: $65

摘要

背景：肌肉减少症的特征是由于衰老或慢性疾病（例如慢性肝病（CLD））而导致肌肉质量和力量的丧失（肌肉萎缩）。骨骼肌萎缩涉及不同的机制，包括减少肌肉纤维直径和肌球蛋白重链水平，增加泛素-蛋白酶体途径活性，氧化应激和肌核细胞凋亡。我们最近发现，除先前研究中未评估的肌核凋亡外，所有这些机制均与与肝毒素5-二乙氧基羰基-1,4-二氢可力丁（DDC）诱导的CLD相关的肌肉萎缩有关。 目的：在本研究中，我们使用补充DDC的饮食喂养小鼠模型评估了CLD相关肌减少症中肌核细胞凋亡的参与以及N-乙酰半胱氨酸（NAC）处理对肌肉力量和细胞凋亡的影响。 方法：在不使用或不使用NAC的情况下，对4个月大的C57BL6雄性小鼠进行标准饮食或DDC补充饮食六周。 结果：我们的结果表明，NAC减轻了补充DDC的饮食喂养小鼠腓肠肌（GA）肌肉中CLD诱导的肌肉消瘦相关的肌肉纤维直径和肌肉强度的降低。此外，与对照饮食喂养的小鼠的GA肌肉相比，DDC补充饮食诱导的CLD喂养的小鼠的GA肌肉表现出增加的肌核凋亡，这由凋亡核数，caspase-8和caspase-9的增加所证明。 caspase-3的表达，酶活性和BAX / BCL-2的比例。 NAC治疗抑制了GA肌肉中与肌核凋亡相关的所有机制。 结论：据我们所知，这是第一篇报道氧化还原调节CLD诱导的少肌症患者肌肉力量和肌核细胞凋亡的研究。

关键词: 肌肉减少症，慢性肝病，肝毒素，UPP氧化应激，细胞凋亡。

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