Liau Y H, Lopez R A, Slomiany A, Slomiany B L
Research Center, New Jersey Dental School, University of Medicine and Dentistry of New Jersey, Newark 07103.
Biochem Biophys Res Commun. 1992 May 15;184(3):1411-7. doi: 10.1016/s0006-291x(05)80040-3.
The effect of H. pylori lipopolysaccharide on the synthesis and secretion of sulfated mucin in gastric mucosa was investigated using mucosal segments incubated in the presence of [3H]proline, [3H]glucosamine and [35S]Na2SO4. The lipopolysaccharide, while showing no discernible effect on the apomucin synthesis was found to inhibit the process of mucin glycosylation and sulfation, which at 100 micrograms/ml lipopolysaccharide reached the optimal inhibition of 65%. The analysis of mucin secretory responses revealed that the lipopolysaccharide by first 15 min caused a 57% stimulation in sulfomucin secretion followed thereafter by inhibition, which reached maximum of 32% by 45 min. The results suggest that colonization of gastric mucosa by H. pylori may be detrimental to the process of gastric sulfomucin synthesis and secretion.
利用在[3H]脯氨酸、[3H]氨基葡萄糖和[35S]硫酸钠存在的情况下孵育的黏膜片段,研究了幽门螺杆菌脂多糖对胃黏膜中硫酸化黏蛋白合成和分泌的影响。结果发现,脂多糖虽然对脱辅基黏蛋白的合成没有明显影响,但却能抑制黏蛋白糖基化和硫酸化过程,在脂多糖浓度为100微克/毫升时,抑制作用达到最佳,为65%。对黏蛋白分泌反应的分析表明,脂多糖在最初15分钟内可使硫酸黏蛋白分泌增加57%,随后出现抑制作用,到45分钟时抑制作用达到最大,为32%。这些结果表明,幽门螺杆菌在胃黏膜的定植可能不利于胃硫酸黏蛋白的合成和分泌过程。