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机构地区:[1]蚌埠医学院药理教研室,安徽233003 [2]蚌埠医学院核医学教研室,安徽233003 [3]蚌埠铁路医院核医学科,安徽233000
出 处:《中国药理学通报》1993年第4期291-294,共4页Chinese Pharmacological Bulletin
摘 要:用碘标记超氧化物歧化酶(^(125)I-SOD)示踪研究牛SOD对RBC膜和实验性小鼠胃溃疡的保护效应。Iodogen固相法^(125)I标记SOD示踪结果表明,^(125)I-SOD经胃肠道能很快被吸收入血,分布于多种脏器,以肾放射性居首位.RBC放射性占全血18.2%(峰值相),血浆结合型放射性仅占12.5%,大部分^(125)I-SOD被解离脱^(125)I。RBC经外源O_2^-自由基的作用证明,SOD有明显抑制O_2^-对RBC膜的氧化损伤作用,并随SOD量增加,其抑制效应亦趋显著.SOD对IM-HCI诱发小鼠胃溃疡的影响,也表现有抑制和保护作用。接受SOD治疗组,粘膜脂质过氧化受抑制,病理变化减轻。This paper reports that the protective effects of SOD on the experimental gastric ulcers in the mice and erythrocyte membranes, as well as the 125I-SOD traced examination to be studied. The radioactive 125I labelling SOD is using by Iodogen solid phase method. The results of traced examination demonstrated that 125I-SOD could be absorbed into the blood rapidly,and distributed to various organs. The renal radioactivity is highest. The radioactivity in erythrocytes (peak phase) has been accounting for 18. 2% in the whole blood. The radioactivity of bound form in the plasma is only accounted for 12. 5%. It shows that the 125I-SOD was mostly degradation and deiodination. The action of the exogenous O2 free radicals on the erythrocytes showed that the SOD have been markedly inhibited the peroxide damage of O2on the erythrocyte membranes, which inhibitory effect was increased with the concentration of the SOD raised. The effect of SOD on the IM-HCI induced the gastric ulcers, an inhibitory and protective action occur too. In the group of SOD treatment, the gastric mucosal membranes lipid peroxidation was inhibited and the pathological changes remited.
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