Bozkurt A, Yüksel M, Haklar G, Kurtel H, Yeğen B C, Alican I
Department of Physiology, Marmara University, School of Medicine, Haydarpaşa, Istanbul, Turkey.
Dig Dis Sci. 1998 Jun;43(6):1258-63. doi: 10.1023/a:1018859824926.
This study examines the putative gastroprotective effect of adenosine on indomethacin-induced gastric lesions and the possible mechanisms involved. After 24 hr of starvation, the rats were treated either with indomethacin (Indo; 25 mg/kg, subcutaneously) alone or adenosine + Indo (Ado; 7.5 mg/kg, subcutaneously, three times a day), or the vehicle (5% NaHCO3, subcutaneously). The length of hemorrhagic lesions in the stomachs was expressed as the lesion index. The tissue-associated myeloperoxidase (MPO) activity and protein oxidation were measured in gastric tissue samples. Formation of reactive oxygen species in gastric tissues was measured by using luminol- and lucigenin-enhanced chemiluminescence. In other groups of rats, gastric mucosal permeability and gastric acid output were performed following the same treatment regimens. The gastric mucosal permeability was measured by determination of [51Cr]EDTA clearance in a perfused stomach preparation and gastric acid secretion studies were performed following pylorus ligation. The lesion index, the increase in lucigenin-enhanced chemiluminescence, and the increase in gastric mucosal permeability in Indo-treated rats were reversed by Ado pretreatment. Ado pretreatment also prevented the increase in gastric acid output and gastric volume in Indo-treated rats. Thus, these findings implicate that exogenous adenosine has a protective role on indomethacin-induced gastric lesions, possibly by inhibiting gastric hyperacidity and reactive oxygen formation and by preventing disruption of the mucosal integrity.
本研究考察了腺苷对吲哚美辛诱导的胃损伤的假定胃保护作用及其可能的作用机制。饥饿24小时后，大鼠分别单独接受吲哚美辛（Indo；25mg/kg，皮下注射）或腺苷+吲哚美辛（Ado；7.5mg/kg，皮下注射，每日三次），或溶剂（5%碳酸氢钠，皮下注射）处理。胃内出血性损伤的长度以损伤指数表示。测定胃组织样本中的组织相关髓过氧化物酶（MPO）活性和蛋白质氧化。通过鲁米诺和光泽精增强化学发光法测定胃组织中活性氧的形成。在其他几组大鼠中，按照相同的处理方案进行胃黏膜通透性和胃酸分泌量的测定。通过测定灌注胃制剂中[51Cr]EDTA清除率来测量胃黏膜通透性，并在幽门结扎后进行胃酸分泌研究。腺苷预处理可逆转吲哚美辛处理大鼠的损伤指数、光泽精增强化学发光的增加以及胃黏膜通透性的增加。腺苷预处理还可防止吲哚美辛处理大鼠胃酸分泌量和胃容积的增加。因此，这些发现表明外源性腺苷对吲哚美辛诱导的胃损伤具有保护作用，可能是通过抑制胃酸过多和活性氧的形成以及防止黏膜完整性的破坏来实现的。
