首页> 外文期刊>Nutrients >The Extract of Arctium lappa L. Fruit (Arctii Fructus) Improves Cancer-Induced Cachexia by Inhibiting Weight Loss of Skeletal Muscle and Adipose Tissue
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The Extract of Arctium lappa L. Fruit (Arctii Fructus) Improves Cancer-Induced Cachexia by Inhibiting Weight Loss of Skeletal Muscle and Adipose Tissue

机译:牛蒡牛蒡子的提取物通过抑制骨骼肌和脂肪组织的体重减轻而改善癌症诱导的恶病症

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Background: Cachexia induced by cancer is a systemic wasting syndrome and it accompanies continuous body weight loss with the exhaustion of skeletal muscle and adipose tissue. Cancer cachexia is not only a problem in itself, but it also reduces the effectiveness of treatments and deteriorates quality of life. However, effective treatments have not been found yet. Although Arctii Fructus (AF) has been studied about several pharmacological effects, there were no reports on its use in cancer cachexia. Methods: To induce cancer cachexia in mice, we inoculated CT-26 cells to BALB/c mice through subcutaneous injection and intraperitoneal injection. To mimic cancer cachexia in vitro, we used conditioned media (CM), which was CT-26 colon cancer cells cultured medium. Results: In in vivo experiments, AF suppressed expression of interleukin (IL)-6 and atrophy of skeletal muscle and adipose tissue. As a result, the administration of AF decreased mortality by preventing weight loss. In adipose tissue, AF decreased expression of uncoupling protein 1 (UCP1) by restoring AMP-activated protein kinase (AMPK) activation. In in vitro model, CM increased muscle degradation factors and decreased adipocytes differentiation factors. However, these tendencies were ameliorated by AF treatment in C2C12 myoblasts and 3T3-L1 cells. Conclusion: Taken together, our study demonstrated that AF could be a therapeutic supplement for patients suffering from cancer cachexia.
机译:背景:癌症诱导的恶病症是一种全身浪费综合征,它伴随着骨骼肌和脂肪组织的耗尽连续体重减轻。癌症恶毒症本身不仅是一个问题,而且还降低了治疗的有效性并降低了生活质量。但是,尚未发现有效的治疗方法。虽然Arctii Fructus(AF)已经研究了几种药理作用,但没有关于其在癌症恶病症中使用的报道。方法:通过皮下注射和腹膜内注射,将CT-26细胞接种CT-26细胞接种CT-26细胞至Balb / C小鼠。为了在体外模仿癌症恶化,我们使用调节培养基(CM),即CT-26结肠癌细胞培养培养基。结果:在体内实验中,AF抑制白细胞介素(IL)-6的表达,骨骼肌和脂肪组织的萎缩。结果,通过预防减肥来施用AF降低的死亡率。在脂肪组织中,AF通过恢复AMP-活化的蛋白激酶(AMPK)活化来降低非偶联蛋白1(UCP1)的表达。在体外模型中,CM增加肌肉降解因子,降低脂肪细胞分化因子。然而,在C2C12肌细胞和3T3-L1细胞中,通过AF治疗来改善这些趋势。结论:在一起,我们的研究表明,AF可以是患有癌症恶病症的患者的治疗补充剂。

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