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硫糖铝对空泡毒素活性及幽门螺杆菌黏附于人胃上皮细胞的影响。

Effects of sucralfate on vacuolating cytotoxin activity and adherence of Helicobacter pylori to human gastric epithelial cells.

作者信息

Smoot D T, Earlington M H, Abebe E, Desbordes B C, Murigande C, Naab T

机构信息

Department of Medicine, Howard University College of Medicine, Washington, DC 20060, USA.

出版信息

J Assoc Acad Minor Phys. 1996;7(4):88-92.

PMID:8936934
Abstract

Sucralfate inhibits activity of certain Helicobacter pylori enzymes, implying that this medication may limit gastric cell injury associated with H pylori infection. This study evaluates the ability of sucralfate and its two major structural components, sucrose octasulfate and aluminum hydroxide, to reduce the cytotoxic effects of H pylori and to inhibit binding of H pylori to human gastric epithelial cells. Experiments were performed using human gastric epithelial cells isolated from gastric biopsy tissue taken at upper gastrointestinal endoscopy. Primary cultures of human gastric epithelial cells, when exposed to broth-culture supernatant from a vacuolating cytotoxin-positive H pylori strain, were shown to form cytoplasmic vacuoles. Preexposing H pylori brothculture supernatant to sucralfate reduced vacuole formation in human gastric epithelial cells; however, preexposure of H pylori broth-culture supernatant to aluminum hydroxide or sucrose octasulfate did not reduce vacuolation in human gastric epithelial cells. H pylori binding to human gastric epithelial cells was significantly reduced when H pylori was exposed to sucralfate prior to incubating the bacterium with human gastric epithelial cells. These data show that sucralfate, but not its two major components, reduces the toxicity of an H pylori-produced cytotoxin (VacA) and decreases H pylori adherence to human gastric epithelial cells. This reduction in H pylori cytotoxicity may contribute to sucralfate's ulcerhealing properties and to the lower ulcer recurrence rates seen in patients treated with this medication.

摘要

硫糖铝可抑制某些幽门螺杆菌酶的活性,这意味着该药物可能会减轻与幽门螺杆菌感染相关的胃细胞损伤。本研究评估了硫糖铝及其两个主要结构成分,即八硫酸蔗糖和氢氧化铝,降低幽门螺杆菌细胞毒性作用以及抑制幽门螺杆菌与人胃上皮细胞结合的能力。实验使用的是人胃上皮细胞,这些细胞是从在上消化道内镜检查时获取的胃活检组织中分离出来的。当人胃上皮细胞原代培养物暴露于来自一株空泡毒素阳性幽门螺杆菌菌株的肉汤培养上清液时,会形成细胞质空泡。将幽门螺杆菌肉汤培养上清液预先与硫糖铝接触,可减少人胃上皮细胞中的空泡形成;然而,将幽门螺杆菌肉汤培养上清液预先与氢氧化铝或八硫酸蔗糖接触,并不会减少人胃上皮细胞中的空泡形成。在将幽门螺杆菌与人胃上皮细胞共同孵育之前,若先将幽门螺杆菌暴露于硫糖铝,则幽门螺杆菌与人胃上皮细胞的结合会显著减少。这些数据表明,硫糖铝而非其两个主要成分,可降低幽门螺杆菌产生的细胞毒素(VacA)的毒性,并减少幽门螺杆菌与人胃上皮细胞的黏附。幽门螺杆菌细胞毒性的这种降低可能有助于硫糖铝的溃疡愈合特性,以及使用该药物治疗的患者中较低的溃疡复发率。

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