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硫糖铝对体外培养的犬上皮细胞产生的黏膜屏障成分的影响。

Effect of sucralfate on components of mucosal barrier produced by cultured canine epithelial cells in vitro.

作者信息

Scheiman J M, Kraus E R, Yoshimura K, Boland C R

机构信息

Research Service, Ann Arbor VA Medical Center, Michigan 48105.

出版信息

Dig Dis Sci. 1992 Dec;37(12):1853-9. doi: 10.1007/BF01308079.

DOI:10.1007/BF01308079
PMID:1473434
Abstract

The mucous gel maintains a neutral microclimate at the epithelial cell surface, which may play a role in both the prevention of gastroduodenal injury and the provision of an environment essential for epithelial restitution and regeneration after injury. Enhancement of the components of the mucous barrier by sucralfate may explain its therapeutic efficacy for upper gastrointestinal tract protection, repair, and healing. We studied the effect of sucralfate and its major soluble component, sucrose octasulfate (SOS), on the synthesis and release of gastric mucin and surface active phospholipid, utilizing an isolated canine gastric mucous cells in culture. We correlated these results with the effect of the agents on mucin synthesis and secretion utilizing explants of canine fundus in vitro. Sucralfate and SOS significantly stimulated phospholipid secretion by isolated canine mucous cells in culture (123% and 112% of control, respectively). Indomethacin pretreatment significantly inhibited the effect of sucralfate, but not SOS, on the stimulation of phospholipid release. Administration of either sucralfate or SOS to the isolated canine mucous cells had no effect upon mucin synthesis or secretion using a sensitive immunoassay. Sucralfate and SOS did not stimulate mucin release in the canine explants; sucralfate significantly stimulated the synthesis of mucin, but only to 108% of that observed in untreated explants. No increase in PGE2 release was observed after sucralfate or SOS exposure to the isolated canine mucous cells. Our results suggest sucralfate affects the mucous barrier largely in a qualitative manner. No increase in mucin secretion or major effect on synthesis was noted, although a significant increase in surface active phospholipid release was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

黏液凝胶在上皮细胞表面维持中性微环境,这可能在预防胃十二指肠损伤以及为损伤后上皮修复和再生提供必要环境方面发挥作用。硫糖铝增强黏液屏障的成分可能解释了其对上消化道保护、修复和愈合的治疗效果。我们利用培养的分离犬胃黏液细胞,研究了硫糖铝及其主要可溶性成分八硫酸蔗糖(SOS)对胃黏液素和表面活性磷脂合成与释放的影响。我们将这些结果与这些药物对体外犬胃底外植体黏液素合成和分泌的影响进行了关联。硫糖铝和SOS显著刺激了培养的分离犬黏液细胞的磷脂分泌(分别为对照的123%和112%)。吲哚美辛预处理显著抑制了硫糖铝对磷脂释放的刺激作用,但对SOS无此作用。使用灵敏的免疫测定法,向分离的犬黏液细胞施用硫糖铝或SOS对黏液素的合成或分泌均无影响。硫糖铝和SOS未刺激犬外植体中的黏液素释放;硫糖铝显著刺激了黏液素的合成,但仅为未处理外植体中观察到的合成量的108%。硫糖铝或SOS作用于分离的犬黏液细胞后,未观察到前列腺素E2释放增加。我们的结果表明,硫糖铝主要以定性方式影响黏液屏障。虽然观察到表面活性磷脂释放显著增加,但未发现黏液素分泌增加或对合成有重大影响。(摘要截短于250字)

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