Nishida K, Ohta Y, Ishiguro I
Department of Biochemistry, School of Medicine, Fujita Health University, Toyoake, Aichi, Japan.
Eur J Pharmacol. 1998 Jul 31;354(1):51-8. doi: 10.1016/s0014-2999(98)00430-0.
We have reported that neutrophil infiltration into gastric mucosa is closely related to gastric mucosal lesion development in rats with water immersion restraint stress. In this study, we examined the effect of teprenone, which is known to prevent gastric mucosal injury through stimulation of gastric mucus synthesis and secretion, on neutrophil infiltration into the gastric mucosa of rats with water immersion restraint stress. Pre- and post-administration of teprenone (200 mg/kg, p.o.) significantly attenuated the neutrophil infiltration into the gastric mucosa and the lesion development found at 6 h of water immersion restraint stress with preservation of gastric mucosal hexosamine and adherent mucus levels. These results indicate that teprenone exerts protective and preventive actions against water immersion restraint stress-induced gastric mucosal lesions in rats and suggest that these actions could be related to the preservation of gastric mucus synthesis and secretion and inhibition of neutrophil infiltration into the gastric mucosal tissue.
我们曾报道，在水浸束缚应激大鼠中，中性粒细胞浸润至胃黏膜与胃黏膜损伤的发展密切相关。在本研究中，我们检测了替普瑞酮对水浸束缚应激大鼠胃黏膜中性粒细胞浸润的影响，已知替普瑞酮可通过刺激胃黏液合成与分泌来预防胃黏膜损伤。替普瑞酮（200mg/kg，口服）给药前后，显著减轻了水浸束缚应激6小时时胃黏膜的中性粒细胞浸润及损伤发展，同时保持了胃黏膜己糖胺和黏附黏液水平。这些结果表明，替普瑞酮对水浸束缚应激诱导的大鼠胃黏膜损伤具有保护和预防作用，并提示这些作用可能与维持胃黏液合成与分泌以及抑制中性粒细胞浸润至胃黏膜组织有关。
