Nosál'ová V, Navarová J
Institute of Experimental Pharmacology, Slovak Academy of Sciences, Bratislava.
Agents Actions. 1994 Jun;41 Spec No:C95-6. doi: 10.1007/BF02007783.
Indomethacin induced gastric damage in rats was accompanied by a decrease in mucosal activities of three lysosomal enzymes tested, with serum levels remaining unchanged. Petreatments with cimetidine (100 mg/kg b.w.) and ranitidine (30 mg/kg b.w.) were found partially to prevent the decrease of N-acetylglucosaminidase and acid phosphatase, as well as of beta-glucuronidase, while the latter was also prevented by famotidine (10 mg/kg b.w.). All the H2 antagonists tested reduced dose-dependently the extent of gastric injury induced by indomethacin and reversed the changes in protein levels. The stabilisation of lysosomal membranes and thus the prevention of lysosomal leakage may be one of the favourable additional mechanisms of antiulcer activity of H2 antagonists.
吲哚美辛诱导的大鼠胃损伤伴随着所检测的三种溶酶体酶的黏膜活性降低，而血清水平保持不变。发现预先用西咪替丁（100毫克/千克体重）和雷尼替丁（30毫克/千克体重）处理可部分预防N-乙酰葡糖胺酶、酸性磷酸酶以及β-葡萄糖醛酸酶的降低，而法莫替丁（10毫克/千克体重）也可预防β-葡萄糖醛酸酶的降低。所有测试的H2拮抗剂均剂量依赖性地降低了吲哚美辛诱导的胃损伤程度，并逆转了蛋白质水平的变化。溶酶体膜的稳定以及由此对溶酶体渗漏的预防可能是H2拮抗剂抗溃疡活性的有利附加机制之一。
