Serrano Aulló M T, Nerín de la Puerta J M, Lanas Arbeloa A I
Servicio de Aparato Digestivo, Hospital Clínico Universitario. Zaragoza.
Rev Esp Enferm Dig. 1996 Apr;88(4):253-7.
The effects of indomethacin on pepsinogen secretion were studied in isolated human peptic cells prepared from endoscopically obtained biopsies after collagenase digestion, mechanical disruption and percoll gradient centrifugation. Low concentrations of indomethacin (10(-8)-10(-10) M) stimulated basal pepsinogen secretion. Higher doses of indomethacin (10(-5)-10(-6) M) potentiated histamine (10(-4) M) and db-cAMP (10(-4) M)-stimulated pepsinogen secretion without affecting acetylcholine (10(-6) M) and CCK-8-stimulated pepsinogen secretion or cell vitality. Increase of pepsinogen secretion was dependent on extracellular calcium because potentiation was abolished by calcium depletion of the medium. We conclude that indomethacin potentiates basal and secretagogue-stimulated pepsinogen secretion by dispersed human peptic cells and this might be an additional mechanism of NSAID-induced gastric injury. This potentiation effect is regulated by calcium and independent of endogenous prostaglandin inhibition.
通过胶原酶消化、机械破碎和Percoll梯度离心从内镜活检组织中制备分离的人胃蛋白酶细胞,研究了吲哚美辛对胃蛋白酶原分泌的影响。低浓度的吲哚美辛(10^(-8)-10^(-10)M)刺激基础胃蛋白酶原分泌。高剂量的吲哚美辛(10^(-5)-10^(-6)M)增强组胺(10^(-4)M)和二丁酰环磷腺苷(10^(-4)M)刺激的胃蛋白酶原分泌,而不影响乙酰胆碱(10^(-6)M)和八肽胆囊收缩素刺激的胃蛋白酶原分泌或细胞活力。胃蛋白酶原分泌的增加依赖于细胞外钙,因为培养基中钙耗尽会消除增强作用。我们得出结论,吲哚美辛增强分散的人胃蛋白酶细胞的基础和促分泌剂刺激的胃蛋白酶原分泌,这可能是非甾体抗炎药诱导胃损伤的另一种机制。这种增强作用受钙调节,且与内源性前列腺素抑制无关。