Ohta Yoshiji, Kamiya Yoshio, Imai Yoichiro, Arisawa Tomiyasu, Nakano Hiroshi
Department of Chemistry, School of Medicine, Fujita Health University, Toyoake, Aichi 470-1192, Japan.
Inflammopharmacology. 2005;13(1-3):249-59. doi: 10.1163/156856005774423881.
We examined the role of gastric mucosal ascorbic acid (AA) in gastric mucosal lesion development in rats with water immersion restraint stress (WIRS). When fasted rats were subjected to WIRS for 1, 3 or 6 h, gastric mucosal lesions developed at 3 and 6 h. Gastric mucosal AA concentration decreased at 3 and 6 h after the onset of WIRS, while gastric mucosal non-protein SH concentration decreased at 1, 3, and 6 h and gastric mucosal vitamin E concentration decreased at 6 h. Gastric mucosal lipid peroxide concentration and myeloperoxidase activity increased at 3 and 6 h of WIRS. Pre-administration of AA (250 mg/kg) prevented gastric mucosal development with attenuation of the decreased gastric mucosal AA, non-protein SH and vitamin E concentrations, and the increased gastric mucosal lipid peroxide concentration and myeloperoxidase activity. These results suggest that gastric mucosal AA plays an important role in WIRS-induced gastric mucosal lesion development.
我们研究了胃黏膜抗坏血酸（AA）在水浸束缚应激（WIRS）大鼠胃黏膜损伤发展中的作用。当禁食大鼠接受1、3或6小时的WIRS时，在3小时和6小时出现胃黏膜损伤。WIRS开始后3小时和6小时，胃黏膜AA浓度降低，而胃黏膜非蛋白巯基浓度在1、3和6小时降低，胃黏膜维生素E浓度在6小时降低。WIRS 3小时和6小时时，胃黏膜脂质过氧化物浓度和髓过氧化物酶活性增加。预先给予AA（250mg/kg）可预防胃黏膜损伤的发展，同时减轻胃黏膜AA、非蛋白巯基和维生素E浓度的降低，以及胃黏膜脂质过氧化物浓度和髓过氧化物酶活性的增加。这些结果表明，胃黏膜AA在WIRS诱导的胃黏膜损伤发展中起重要作用。
