Polysaccharides from Capsosiphon fulvescens Stimulate the Growth of IEC-6 Cells by Activating the MAPK Signaling Pathway
Polysaccharides from Capsosiphon fulvescens Stimulate the Growth of IEC-6 Cells by Activating the MAPK Signaling Pathway
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DOI：
10.1007/s10126-010-9314-y
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发表时间：
2011-06-01
影响因子：
3
通讯作者：
Taek-Jeong Nam
中科院分区：
文献类型：
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作者：
Go, Hiroe;Hwang, Hye-Jung;Taek-Jeong Nam
海藻提取物表现出多种生物活性，例如抗氧化和抗肿瘤活性。 Capsosiphon fulvescens 是一种绿藻，在韩国西南海岸盛产。尽管它因其所谓的增强健康特性而被食用，特别是作为治疗胃部疾病和宿醉的药物，但膳食中的 C. fulvescens 对健康的影响仍不清楚。我们从 C. fulvescens (Cf-PS) 中提取多糖，研究其对大鼠小肠上皮 IEC-6 细胞增殖的影响，并确定所涉及的信号级联。我们在 Cf-PS 存在下培养 IEC-6 细胞，Cf-PS 以剂量依赖性方式刺激细胞增殖，并分析与细胞增殖相关的 Wnt 和 MAPK 信号通路。 Cf-PS 处理诱导β-连环蛋白（Wnt 信号通路的效应子）从细胞质易位到细胞核，并增加了 cyclinD1 和 c-myc 的表达。 Cf-PS 还诱导 ERK1/2 磷酸化，该磷酸化可被生长因子等促有丝分裂和增殖刺激激活，但 JNK 和 p38 的磷酸化并未增强。我们的结果表明，Cf-PS 通过刺激肠上皮细胞中 β-catenin 的核转位和 ERK1/2 激活来调节增殖。
Seaweed extracts show diverse bioactivities, such as antioxidant and antitumor activity. Capsosiphon fulvescens is a green alga that is abundant along the southwest coast of South Korea. Although it is consumed for its purported health-enhancing properties, particularly as a treatment for stomach disorders and hangovers, the health effects of dietary C. fulvescens remain unclear. We extracted polysaccharides from C. fulvescens (Cf-PS), investigated their effects on the proliferation of rat small intestinal epithelial IEC-6 cells, and determined the signaling cascade involved. We cultured IEC-6 cells in the presence of Cf-PS, which stimulated cell proliferation in a dose-dependent manner, and analyzed the Wnt and MAPK signaling pathways, which are related to cell proliferation. Cf-PS treatment induced the translocation of beta-catenin, an effector of the Wnt signaling pathway, from the cytosol to the nucleus and increased the expression of cyclinD1 and c-myc. Cf-PS also induced ERK1/2 phosphorylation, which is activated by mitogenic and proliferative stimuli such as growth factors, but the phosphorylation of JNK and p38 was not enhanced. Our results show that Cf-PS regulates proliferation via stimulating the nuclear translocation of beta-catenin and ERK1/2 activation in intestinal epithelial cells.