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首页> 外文期刊>Life sciences >Fucoidan, a sulfated polysaccharide, inhibits adipogenesis through the mitogen-activated protein kinase pathway in 3T3-L1 preadipocytes.
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Fucoidan, a sulfated polysaccharide, inhibits adipogenesis through the mitogen-activated protein kinase pathway in 3T3-L1 preadipocytes.

机译：Fucoidan是一种硫酸化多糖，可通过3T3-L1前脂肪细胞中的促分裂原激活的蛋白激酶途径抑制脂肪形成。

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AIMS: Fucoidan, consisting of L-fucose together with xylose, galactose and mannose, is a sulfated polysaccharide from brown seaweeds, which has been reported to affect the development of adipocytes. However, the role of fucoidan in adipogenesis remains elusive. In the present study, we have investigated the inhibitory effects of fucoidan on adipocyte differentiation via mitogen-activated protein kinase (MAPK) signaling pathway in 3T3-L1 preadipocytes. MAIN METHODS: Differentiation of 3T3-L1 preadipocytes was induced in the presence or absence of fucoidan. The effects of fucoidan on adipogenic gene expression and MAPK activation were investigated. KEY FINDINGS: Fucoidan treatment inhibits adipocyte differentiation, evidenced by decreased lipid accumulation and down regulation of adipocyte markers. Fucoidan then inhibited the expression of both early CCAAT-enhancer-binding proteins alpha (C/EBPalpha) and peroxisome proliferator-activated receptors gamma (PPARgamma) and late activating protein 2 (aP2) adipogenic transcription factors, which is a crucial role for adipocyte development. Moreover, our results revealed that fucoidan inhibited the early activation of p38 MAPKs, extracellular signal-regulated kinases (ERK) and Jun N-terminal kinase (JNK). SIGNIFICANCE: Overall, these findings are a strong indication that fucoidan might inhibit adipogenesis in 3T3-L1 preadipocytes, due to inhibition of the MAPK signaling pathway that involves adipogenic transcription factors.
机译：目的：岩藻糖聚糖由L-岩藻糖以及木糖，半乳糖和甘露糖组成，是一种褐藻海藻中的硫酸化多糖，据报道会影响脂肪细胞的发育。然而，岩藻依聚糖在脂肪形成中的作用仍然难以捉摸。在本研究中，我们已经研究了岩藻依聚糖通过3T3-L1前脂肪细胞中的促分裂原活化蛋白激酶（MAPK）信号传导途径对脂肪细胞分化的抑制作用。主要方法：在存在或不存在岩藻依聚糖的情况下诱导3T3-L1前脂肪细胞的分化。研究了岩藻依聚糖对成脂基因表达和MAPK激活的影响。主要发现：岩藻依聚糖治疗可抑制脂肪细胞分化，这通过减少脂质蓄积和降低脂肪细胞标志物来证明。 Fucoidan然后抑制早期CCAAT增强子结合蛋白α（C / EBPalpha）和过氧化物酶体增殖物激活受体γ（PPARgamma）和晚期激活蛋白2（aP2）成脂转录因子的表达，这对脂肪细胞发育至关重要。此外，我们的研究结果表明，岩藻依聚糖能抑制p38 MAPK，细胞外信号调节激酶（ERK）和Jun N末端激酶（JNK）的早期活化。意义：总体而言，这些发现强烈表明岩藻依聚糖可能会抑制3T3-L1前脂肪细胞中的脂肪生成，这是由于涉及脂肪形成转录因子的MAPK信号通路受到抑制。

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