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《营养科学》杂志揭示岩藻多糖抑制幽门螺杆菌与胃黏膜黏附机制
发表时间:2020-06-19         作者:岩藻多糖         来源:J Nutr Sci Vitaminol, 1999, 45, 325-336        
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原标题:海蕴岩藻多糖具有抑制幽门螺杆菌与胃黏膜上皮细胞黏附作用

①70%的胃溃疡患者、50-60%的慢性胃炎患者及90%的十二指肠溃疡患者体内都感染幽门螺杆菌,幽门螺杆菌也是慢性胃炎发展为胃癌的重要影响因素。幽门螺杆菌致病机制第一步是,幽门螺杆菌能穿过为胃粘液层,与胃上皮细胞粘附,因此如何阻止幽门螺杆菌与胃上皮细胞黏附是抗幽门螺杆菌的关键。
②岩藻多糖是来自于褐藻表面黏液的大分子多糖物质,主要活性基团为硫酸基和岩藻糖,具有很强的结合幽门螺杆菌作用。
③实验结果:岩藻多糖能够抑制幽门螺杆菌与胃黏膜上皮细胞(MKN28、KATO III)的黏附 (IC50=16-30mg/mL),硫酸葡聚糖和岩藻糖没有抑制作用。
④Western blot(蛋白印迹)实验结果发现,幽门螺杆菌表面含有岩藻多糖结合蛋白,未发现其他多糖结合蛋白,因此揭示了岩藻多糖抑制幽门螺杆菌与胃黏膜黏附的作用机理。
⑤结论:只有岩藻多糖(同时具有硫酸基和岩藻糖)具有很强的结合幽门螺杆菌,抑制幽门螺杆菌与胃黏膜上皮细胞黏附的作用,其他含硫酸基的多糖(如硫酸葡聚糖)或岩藻糖(单糖)没有抑制效果;抑制黏附的作用机制是幽门螺杆菌表面含有岩藻多糖结合蛋白,可以特异性地与岩藻多糖结合,从而抑制幽门螺杆菌与胃黏膜的黏附。

延伸阅读
J Nutr Sci Vitaminol, 1999, 45, 325-336
Inhibitory Effect of Cladosiphon Fucoidan on the Adhesion of Helicobacter pylori to Human Gastric Cells
Abstract:
We studied the inhibitory effect of Cladosiphon fucoidan on the attachment of Helicobacter pylori (H. pylori), a gastroduodenal pathogen, to human gastric cell lines. The bacterial binding in these cell lines was inhibited more by Cladosiphon fucoidan (IC50=16-30mg/mL), than by the fucoidan from Fucus (IC50>30mg/mL). Dextran sulfate, another sulfated polysaccharide, did not inhibit the binding at all. Pre-incubating the bacterial suspension with fucoidans reinforced the inhibitory ability of these components, and reduced the IC50 value of Cladosiphon fucoidan to approximately 1mg/mL. However, the binding was not inhibited by pre-treatment of gastric cells with these com ponents. It was also shown that this fucoidan blocks both Leb and sulfatide-mediated attachment of H. pylori to gastric cells. Furthermore, fucoidan-binding proteins were found on the H. pylori cell surface by Western blot analysis. Thus, the inhibitory effect exerted by Cladosiphon fucoidan on binding between H. pylori and gastric cells might result from
the coating with this component of the bacterial surface.
First Authors:
Hideyuki SHIBATA 
Correspondence:
Teruo YOKOKURA 
All Authors:
Hideyuki SHIBATA, Itsuko KIMURA-TAKAGI, Masato NAGAOKA, Shusuke HASHIMOTO, Haruji SAWADA, Sadao UEYAMA and Teruo YOKOKURA
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