【摘要】 目的　建立大鼠 D-半乳糖衰老模型 ,检测其脑、胃、肝、大肠、小肠细胞浆及线粒体自由基代谢相关指标 (SOD、CAT、XOD、MDA、ONOO- )。方法　引用模糊综合分析的数理统计方法 ,与对照组比较 ,对以上脏器细胞浆及线粒体自由基代谢相关指标进行模糊综合分析。结果　发现线粒体 SOD、CAT、XOD、MDA、ONOO-的综合作用对衰老有影响 ,影响程度为 45% ;而细胞浆 SOD、CAT、XOD、MDA、ONOO-的综合作用对衰老影响较小 ,影响程度为 40 %。通过检测脑细胞蛋白质羰基含量 ,发现该模型脑细胞蛋白质羰基含量显著升高 ,经中药复方治疗后其脑细胞浆蛋白质的羰基含量明显降低。结论　自由基代谢变化可能仅是 D-半乳糖衰老大鼠的表现或机理之一 ,说明自由基衰老理论不能完美解释该模型。初步认为该模型可能包含羰基毒化机制。自由基代谢的改变可能是脑细胞蛋白质羰基化的主要原因 ,此外 D-半乳糖衰本身亦可能致该模型大鼠脑细胞蛋白质羰基化更多还原

【Abstract】 ? Objective To establish the rat aging model by D galactose and determine the correlated markers of the free radical metabolism. MethodsThe rat aging models were established by injection of D galactose and the related markers of the free radical metabolism (SOD?CAT?XOD?MDA?ONOO) from mitochondria and cell plasma were detected in brain, stomach, liver, large intestine and small intestine with fuzzy statistical method. Results The markers (SOD?CAT?XOD?MDA?ONOO) in mitochondria and cell plasma had effects on aging at a degree of 45% and 40%,respectively.In addition, the protein carbonyl toxification was found in the brain cell plasma by detecting formation of protein hydrazone derivation on treatment with 2,4 dinitrophenylhydrazine. Conclusion Our results suggest that there are carbonyl toxification in the rat aging models induced by D galactose. Maybe, Free radicals mainly account for this change, but the D galactose itself can also lead to carbonyl toxification.更多还原