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目的 分析D -半乳糖衰老模型大鼠主要脏器自由基代谢状况 ,初步探讨该模型的羰基毒化机理。方法 以D -半乳糖头颈部皮下注射 ,制造大鼠衰老模型 ,检测相应脏器组织细胞及线粒体丙二醛、超氧化物歧化酶、过氧化氢酶 ,并进行模糊综合分析 ,同时对相应脏器细胞蛋白质的羰基毒化进行初步鉴定。结果 发现该模型鼠脑胶质细胞增生 (形成胶质小结 )、肝脂肪变性、胃肠炎性细胞浸润、粘膜糜烂及其衰老改变 ;发现D -半乳糖致大鼠衰老与线粒体丙二醛升高、超氧化物歧化酶及过氧化氢酶降低均相关 ,相关程度为 4 5 % ,与细胞丙二醛、超氧化物歧化酶、过氧化氢酶亦相关 ,相关程度为 4 0 %。羰基化鉴定发现 ,D -半乳糖模型鼠的脑、胃、肝细胞蛋白质有显著的羰基化。结论 初步认为D -半乳糖致大鼠衰老可能是通过羰 -氨反应 ,形成交联产物 ,通过羰基毒化机制致使大鼠体内蛋白质功能丧失 ,进而引起一系列的衰老改变。交联产物进一步降解可生成丙二醛等不饱和醛酮中间产物 ,因而D -半乳糖衰老模型大鼠各主要脏器细胞质或线粒体丙二醛浓度升高
OBJECTIVE: To analyze the metabolism of free radicals in the major organs of D-galactose-induced aging rats and to explore the mechanism of carbonyl poisoning in this model. Methods The rat model of aging was established by subcutaneous injection of D - galactose into the head and neck of the rats to detect the malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (MDA) in mitochondria of the corresponding viscera and the fuzzy comprehensive analysis. At the same time, Carbonyl poisoning of visceral cellular proteins was initially identified. The results showed that glial cell proliferation (glial formation), hepatic steatosis, gastrointestinal inflammatory cell infiltration, mucosal erosion and senescence were found in this model rat. It was found that aging of D - galactose induced mitochondrial malondialdehyde High, superoxide dismutase and catalase decreased correlation, the degree of correlation was 45%, and cell MDA, SOD, catalase also related, the degree of correlation was 40%. Carbonylation identification showed that D - galactose model mice had significant carbonylation of protein in the brain, stomach and liver cells. Conclusion It is preliminarily believed that the senescence induced by D - galactose may result in the formation of a cross - linked product through the carbonyl - ammonia reaction, resulting in the loss of protein function in rats through the carbonyl poisoning mechanism, leading to a series of aging changes. Further degradation of the cross - linked product can generate unsaturated aldehyde and ketone intermediates such as malondialdehyde, and thus the cytoplasm or mitochondrial MDA level in D - galactose senescent model rats increased