Nishida K, Ohta Y, Ishiguro I
Department of Biochemistry, School of Medicine, Fujita Health University, Aichi, Japan.
Res Commun Mol Pathol Pharmacol. 1998 May;100(2):201-12.
In rats with gastric mucosal lesions induced by water immersion restraint (WIR) stress over a 6 h period, increases in the serum and gastric mucosal concentrations of nitrite/nitrate, the breakdown products of NO, occurred with a drastic increase in inducible NO synthase (iNOS) activity in the gastric mucosa. Pretreatment with aminoguanidine (100 mg/kg), a relatively selective iNOS inhibitor, attenuated not only gastric mucosal lesion development, but also increases in serum and gastric mucosal nitrite/nitrate concentrations with inhibition of increased gastric mucosal iNOS activity in rats with 6 h of WIR stress. A good positive correlation between either serum or gastric mucosal nitrite/nitrate concentration and gastric mucosal iNOS activity in all rats used (r = 0.741 or 0.842, respectively, p < 0.001) was found. These results suggest that in WIR-stressed rats, an increase in NO production via iNOS in the gastric mucosa could contribute to gastric mucosal lesion development.
在通过水浸束缚(WIR)应激诱导胃黏膜损伤6小时的大鼠中,血清和胃黏膜中亚硝酸盐/硝酸盐(NO的分解产物)的浓度增加,同时胃黏膜中诱导型一氧化氮合酶(iNOS)的活性急剧增加。用相对选择性的iNOS抑制剂氨基胍(100mg/kg)预处理,不仅减弱了胃黏膜损伤的发展,还抑制了在6小时WIR应激大鼠中血清和胃黏膜亚硝酸盐/硝酸盐浓度的增加以及胃黏膜iNOS活性的升高。在所使用的所有大鼠中,血清或胃黏膜亚硝酸盐/硝酸盐浓度与胃黏膜iNOS活性之间均存在良好的正相关(r分别为0.741或0.842,p<0.001)。这些结果表明,在WIR应激的大鼠中,胃黏膜中通过iNOS产生的NO增加可能促进胃黏膜损伤的发展。