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研究地高辛抗血清对缺血再灌注脑损伤的拮抗作用 ,采用了大鼠全脑缺血再灌注模型 ,比色法检测脑匀浆液中超氧化物歧化酶 (SOD)活性、丙二醛 (MDA)含量、脑细胞膜Na+ K+ 交换ATP酶活性、血清肌酸激酶(CK)含量 ;用放射免疫法检测脑匀浆液中内洋地黄素含量。结果发现 ,全脑缺血再灌注导致脑组织SOD活性和ATP酶活性显著下降 ,脑组织MDA水平、内洋地黄素水平和血清CK水平显著升高。地高辛抗血清能改善由于脑缺血再灌注所造成的SOD、ATP酶活性的下降以及MDA、CK和内洋地黄素水平的升高。结果表明 ,地高辛抗血清对脑缺血再灌注脑损伤具有保护作用 ,其作用机制与减轻脂质过氧化、促进自由基的清除以及改善脑能量代谢有关。这些作用可能是通过拮抗内洋地黄素的作用而实现的。
To study the antagonism of digoxin antiserum on brain injury induced by ischemia-reperfusion, the model of global cerebral ischemia / reperfusion in rats was established. The activity of superoxide dismutase (SOD), malondialdehyde (MDA) MDA content, Na + K + exchange ATPase activity in brain cell membrane and creatine kinase (CK) content in brain were measured. Content of endoxin in cerebral homogenate was detected by radioimmunoassay. The results showed that global cerebral ischemia-reperfusion led to a significant decrease in brain SOD activity and ATPase activity, brain MDA levels, endoxin and serum CK levels were significantly increased. Anti-digoxin antiserum can reduce the activity of SOD and ATPase and the increase of MDA, CK and endoxin in cerebral ischemia and reperfusion. The results showed that anti-digoxin antiserum had a protective effect on brain injury induced by cerebral ischemia-reperfusion. Its mechanism was related to the reduction of lipid peroxidation, the promotion of free radical scavenging and the improvement of brain energy metabolism. These effects may be achieved by antagonizing the effects of endoxin.