Mechanisms of action of sucralfate.
Mechanisms of action of sucralfate.
复制标题
硫糖铝的作用机制。
DOI：
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发表时间：
1981
影响因子：
2.9
通讯作者：
R. Nagashima
中科院分区：
文献类型：
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作者：
R. Nagashima
硫糖铝与十二指肠溃疡和胃溃疡以及乙醇和抗炎药引起的胃糜烂结合。硫糖铝对有缺陷的粘膜的亲和力可以通过药物的粘性和带负电荷的硫糖铝聚阴离子与粘膜病变中高浓度存在的带正电荷的蛋白质之间形成多价桥来解释。硫糖铝还可以缓冲酸、抑制胃蛋白酶的作用并吸附胆汁盐。硫糖铝的这些特性使药物能够作为酸、胃蛋白酶和胆汁盐渗透的有效屏障。证据支持这样一个全面的保护屏障效应。硫糖铝也与未损伤的粘膜结合，并被认为对再生和正常粘膜发挥类似的“屏障”作用。硫糖铝抗溃疡作用的其他可能机制包括从胃分泌物中消耗酸、胃蛋白酶和胆汁盐。动物数据表明，硫糖铝的作用是持续的，因为它的粘性，与酸反应慢，和有缺陷的粘膜的高亲和力。
Sucralfate binds to duodenal and gastric ulcers and to gastric erosions produced by ethanol and anti-inflammatory drugs. The affinity of sucralfate for defective mucosa is explained by the drug's viscous adhesiveness and the formation of polyvalent bridges between the negatively charged sucralfate polyanions and positively charged proteins present in high concentrations in mucosal lesions. Sucralfate also buffers acid, inhibits the action of pepsin, and adsorbs bile salts. These properties of sucralfate enable the drug to act as an effective barrier to the penetration of acid, pepsin, and bile salts. Evidence to support such a comprehensive protective barrier effect is presented. Sucralfate also binds to uninjured mucosa and is believed to exert a similar "barrier" effect on regenerated and normal mucosa. Other possible mechanism for sucralfate's antiulcer effect include depletion of acid, pepsin, and bile salts from the the gastric secretion. Animal data show that the action of sucralfate is sustained because of its viscous adhesiveness, slow reaction with acid, and high affinity for defective mucosa.