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首页> 外文期刊>The Journal of Nutritional Biochemistry >PPAR gamma as a molecular target of EPA anti-inflammatory activity during TNF- alpha-impaired skeletal muscle cell differentiation.
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PPAR gamma as a molecular target of EPA anti-inflammatory activity during TNF- alpha-impaired skeletal muscle cell differentiation.

机译：PPARγ是TNF-α损伤的骨骼肌细胞分化过程中EPA抗炎活性的分子靶标。

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Activated skeletal muscle satellite cells facilitate muscle repair or growth through proliferation, differentiation and fusion into new or existing myotubes. Elevated levels of the proinflammatory cytokine tumor necrosis factor- alpha (TNF- alpha) impair this process and are documented to have significant roles in muscle pathology. Recent evidence shows that the omega-3 polyunsaturated fatty acid eicosapentaenoic acid (EPA) can block TNF-mediated suppression of progenitor cell differentiation, but the nature of this activity and its significance for local regulation of inflammation are not known. In the current study, we examined differentiation of the C2C12 myoblast line during treatment with TNF- alpha and EPA and measured the expression, activation and inhibition of peroxisome proliferator-activated receptor- gamma (PPAR gamma), as several studies have shown its involvement in mediating EPA activity and the inhibition of nuclear factor (NF)- kappaB inflammatory gene activation. We found that TNF- alpha treatment increased NF- kappaB activity and reduced expression and activation of PPAR gamma, resulting in impaired myotube formation. EPA treatment attenuated these effects of TNF- alpha and was associated with up-regulation of PPAR gamma. Furthermore, EPA inhibited TNF- alpha-mediated transcription and secretion of interleukin (IL)-6, a key target gene of TNF-mediated NF- kappaB transcriptional activity. Pretreatment with a PPAR gamma selective antagonist inhibited some of the actions of EPA but was only partially effective in reversing inhibition of IL-6 production. These results show that EPA activity was associated with altered expression and activation of PPAR gamma, but exerted through both PPAR gamma-dependent and PPAR gamma-independent pathways leading to suppression of the proinflammatory cellular microenvironment
机译：活化的骨骼肌卫星细胞通过增殖，分化和融合成新的或现有的肌管，促进肌肉修复或生长。促炎性细胞因子肿瘤坏死因子-α（TNF-α）的升高水平损害了这一过程，并据报道在肌肉病理学中具有重要作用。最近的证据表明，omega-3多不饱和脂肪酸二十碳五烯酸（EPA）可以阻断TNF介导的祖细胞分化抑制，但是这种活性的性质及其对炎症的局部调节作用尚不清楚。在本研究中，我们检查了C2C12成肌细胞系在TNF-α和EPA治疗期间的分化，并测量了过氧化物酶体增殖物激活的受体-γ（PPARγ）的表达，激活和抑制，因为一些研究表明其参与了介导EPA活性和抑制核因子（NF）-κB炎症基因激活。我们发现，TNF-α处理可增加NF- kappaB活性，并降低PPARγ的表达和激活，从而导致肌管形成受损。 EPA处理减弱了TNF-α的这些作用，并与PPARγ的上调有关。此外，EPA抑制了TNF-α介导的转录和白介素（IL）-6的分泌，白介素是TNF介导的NF-κB转录活性的关键靶基因。用PPARγ选择性拮抗剂进行预处理可抑制EPA的某些作用，但仅能部分有效地逆转对IL-6产生的抑制作用。这些结果表明，EPA活性与PPARγ的表达和激活改变有关，但通过PPARγ依赖性和PPARγ依赖性途径发挥作用，从而抑制促炎性细胞微环境。

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