论文部分内容阅读
将３２只新西兰种幼兔随机分为对照组、室息组、窒息＋ＳＯＤ组。各组均于实验开始后２４小时心脏取血查ＬＰＯ、ＳＯＤ和ＧＳＨ－Ｐｘ、并取脑组织测脑水分含量。窒息组与对照组比较，血清ＬＰＯ、脑水分含量明显增高、（Ｐ均＜０．０１），血中ＳＯＤ、ＧＳＨ－ＰＸ活性明显降低（Ｐ均＜０．０１），窒息组ＬＰＯ与脑水分含量呈正相关关系。室息＋ＳＯＤ组与室息组比较，血清ＬＰＯ、脑水分含量明显减少（Ｐ均＜０．０１），ＧＳＨ－Ｐｘ活性增高（Ｐ＜０．０１）。提示ＯＦＲ参与了窒息所致脑损伤的病理过程，外源性ＳＯＤ可对室息幼兔脑组织起保护作用。
Thirty-two New Zealand seedlings were randomly divided into control group, Ruoxi group, choking + SOD group. Blood samples were taken from the heart of each group for LPO, SOD and GSH-Px 24 hours after the start of the experiment, and brain water content was measured. Compared with the control group, the levels of serum LPO and brain water in the asphyxia group were significantly increased (P <0.01) and the activities of SOD and GSH-PX in the blood were significantly decreased (all P <0.01) Content was positively correlated. Serum LPO and brain water content decreased significantly (P <0.01) and GSH-Px activity increased (P <0.01). It is suggested that OFR is involved in the pathological process of asphyxial brain injury. Exogenous SOD may play a protective role in the brain tissue of infants and young children.