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薯蓣皂苷元可减轻脂肪细胞与巨噬细胞相互作用中的炎症变化。

Diosgenin attenuates inflammatory changes in the interaction between adipocytes and macrophages.

机构信息

Laboratory of Molecular Function of Food, Division of Food Science and Biotechnology, Graduate School of Agriculture, Kyoto University, Uji, Kyoto, Japan.

出版信息

Mol Nutr Food Res. 2010 Jun;54(6):797-804. doi: 10.1002/mnfr.200900208.

Abstract

Obese adipose tissues are characterized by the enhanced infiltration of macrophages. It is considered that the paracrine loop involving monocyte chemoattractant protein-1, tumor necrosis factor-alpha, and the free fatty acid between adipocytes and macrophages establishes a vicious cycle that aggravates inflammatory changes and insulin resistance in obese adipose tissues. Diosgenin, a saponin aglycon found in a variety of plants, has anti-inflammatory properties. In the present study, we examined the effect of diosgenin on the inflammatory changes in the interaction between adipocytes and macrophages. A coculture of 3T3-L1 adipocytes and RAW 264 macrophages markedly enhanced the production of tumor necrosis factor-alpha, monocyte chemoattractant protein-1, and nitric oxide compared with the sum of their single cultures; however, treatment with diosgenin inhibited the production of these proinflammatory mediators. Diosgenin also suppressed the inflammation in RAW 264 macrophages that was induced by the conditioned medium derived from 3T3-L1 adipocytes. Furthermore, diosgenin inhibited the conditioned medium-induced degradation of inhibitor kappaB and the phosphorylation of c-jun N-terminal kinase in macrophages. These results indicate that diosgenin exhibits anti-inflammatory properties in the interaction of adipocytes and macrophages by inhibiting the inflammatory signals in macrophages. Diosgenin may be useful for ameliorating the inflammatory changes in obese adipose tissues.

摘要

肥胖脂肪组织的特征是巨噬细胞的浸润增强。人们认为,脂肪细胞和巨噬细胞之间涉及单核细胞趋化蛋白-1、肿瘤坏死因子-α和游离脂肪酸的旁分泌环建立了一个恶性循环,加剧了肥胖脂肪组织中的炎症变化和胰岛素抵抗。薯蓣皂苷元是一种存在于多种植物中的甾体皂苷配基,具有抗炎特性。在本研究中,我们研究了薯蓣皂苷元对脂肪细胞和巨噬细胞相互作用中炎症变化的影响。与单一培养相比,3T3-L1 脂肪细胞和 RAW 264 巨噬细胞的共培养显著增加了肿瘤坏死因子-α、单核细胞趋化蛋白-1 和一氧化氮的产生;然而,薯蓣皂苷元抑制了这些促炎介质的产生。薯蓣皂苷元还抑制了由 3T3-L1 脂肪细胞衍生的条件培养基诱导的 RAW 264 巨噬细胞的炎症。此外,薯蓣皂苷元抑制了条件培养基诱导的巨噬细胞中抑制剂 kappaB 的降解和 c-jun N-末端激酶的磷酸化。这些结果表明,薯蓣皂苷元通过抑制巨噬细胞中的炎症信号,在脂肪细胞和巨噬细胞的相互作用中表现出抗炎特性。薯蓣皂苷元可能有助于改善肥胖脂肪组织中的炎症变化。

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