Yoshikawa T, Naito Y, Tanigawa T, Yoneta T, Yasuda M, Ueda S, Oyamada H, Kondo M
First Department of Medicine, Kyoto Prefectural University of Medicine, Japan.
Free Radic Res Commun. 1991;14(4):289-96. doi: 10.3109/10715769109088958.
The protective effect of a novel synthetic zinc-carnosine chelate compound, zinc N-(3-aminopropionyl)-L-histidine (Z-103), on the gastric mucosal injury induced by ischemia-reperfusion was studied in rats. Ischemia and reperfusion injury was produced on the rat stomach by applying a small clamp to the celiac artery for 30 min and by removal of the clamp for 30 min. The decrease in the gastric mucosal blood flow was not influenced by the treatment with Z-103. The increase in total area of the erosions on the stomach after ischemia-reperfusion and the increase in lipid peroxides in the gastric mucosa were significantly inhibited by the oral administration of Z-103. In addition, Z-103 inhibited lipid peroxidation of rat brain homogenate and liver microsome in vitro. These results suggest that the protective effect of Z-103 against the aggravation of gastric mucosal injury induced by ischemia-reperfusion may be due to its inhibitory effect on lipid peroxidation.
在大鼠中研究了一种新型合成锌 - 肌肽螯合物,N -(3 - 氨丙酰基)-L - 组氨酸锌(Z - 103)对缺血再灌注诱导的胃黏膜损伤的保护作用。通过用小夹子夹闭腹腔动脉30分钟并移除夹子30分钟来造成大鼠胃的缺血和再灌注损伤。胃黏膜血流量的减少不受Z - 103处理的影响。口服Z - 103可显著抑制缺血再灌注后胃糜烂总面积的增加以及胃黏膜中脂质过氧化物的增加。此外,Z - 103在体外抑制大鼠脑匀浆和肝微粒体的脂质过氧化。这些结果表明,Z - 103对缺血再灌注诱导的胃黏膜损伤加重的保护作用可能归因于其对脂质过氧化的抑制作用。