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首页> 外文期刊>Phytotherapy research: PTR >Isobavachalcone attenuates myotube atrophy induced by TNF-alpha through muscle atrophy F-box signaling and the nuclear factor erythroid 2-related factor 2 cascade
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Isobavachalcone attenuates myotube atrophy induced by TNF-alpha through muscle atrophy F-box signaling and the nuclear factor erythroid 2-related factor 2 cascade

机译:Isobavachalcone通过肌肉萎缩F盒信号传导和核因子红外2相关系数2级联,抑制TNF-α诱导的肌室萎缩萎缩

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摘要

Skeletal muscle atrophy is a condition characterized by damaged muscle fibers and reduced numbers of muscle cells due to various causes. Muscle atrophy is associated with chronic diseases, such as heart failure, diabetes, and aging-related diseases. Isobavachalcone (IBC) is a flavonoid found in various foods and natural products, and studies have investigated its diverse effects, including its neuroprotective and anticancer effects. However, no studies have evaluated the effects of IBC on muscle atrophy. Thus, in this study, we assessed the effects of IBC on prevention of muscle atrophy. To evaluate the preventive effects of IBC on muscle atrophy, we used C2C12 myoblasts and induced muscle atrophy by tumor necrosis factor (TNF)-alpha. IBC regulated the expression levels of muscle atrophy F-box and muscle RING finger-1 in response to damaged muscle cells, thereby restoring the expression of myosin heavy chain and myogenin. Moreover, IBC regulated the phosphorylation of the nuclear factor-kappa B and p38 and upregulated the expression of nuclear factor erythroid 2-related factor 2 and heme oxygenase-1, which are involved in regulating oxidative stress. Our results indicated that IBC acted to relieve TNF-alpha-induced skeletal muscle atrophy by regulating the factors related to inflammation and oxidative stress.
机译:骨骼肌萎缩是由于各种原因,肌肉纤维受损和减少肌肉细胞数量的病症。肌肉萎缩与慢性疾病有关,如心力衰竭,糖尿病和衰老相关疾病。 Isobavachalcone(IBC)是在各种食品和天然产品中发现的黄酮类化合物,研究研究了其各种影响,包括其神经保护和抗癌效果。然而,没有研究评估IBC对肌萎缩的影响。因此,在本研究中,我们评估了IBC对预防肌萎缩的影响。为了评估IBC对肌肉萎缩的预防效果,我们使用C2C12肌细胞并通过肿瘤坏死因子(TNF) - alpha诱导肌肉萎缩。 IBC响应受损肌肉细胞响应肌肉萎缩F箱和肌肉环手指1的表达水平,从而恢复肌球蛋白重链和肌原素的表达。此外,IBC调节核因子-Kappa B和P38的磷酸化,并上调核因子红外2相关因子2和血红素氧酶-1的表达,其参与调节氧化应激。我们的结果表明,IBC通过调节与炎症和氧化应激相关的因素来抑制TNF-α诱导的骨骼肌萎缩。

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