论文部分内容阅读
目的:探讨新生大鼠缺氧缺血脑损伤(HIBD)后细胞凋亡与自由基损伤机制的研究。方法:7日龄SD大鼠72只,随机分成6组:①正常对照组;②HIBD后0h组;③HIBD后24h组;④HIBD后48h组;⑤HIBD后72h组;⑥HIBD后7d组。制备HIBD模型后0,24,48,72h,7d后处死大鼠,取脑并检测脑组织中超氧化物歧化酶(SOD)、丙二醛(MDA)水平;并作HE和Tunel染色光镜下检测各组脑细胞凋亡数。结果:HIBD后各组脑组织SOD,MDA水平及脑细胞凋亡数与对照组比较均有显著性差异,48h及72h组与其他组比较有显著性差异;48h与72h组之间比较无显著性差异。结论:新生大鼠HIBD后48~72h为脑损伤高峰期,细胞凋亡与自由基损伤均参与了缺氧缺血后神经细胞的损害,阻止细胞凋亡或抗自由基损伤应争取在48h内进行。
Objective: To investigate the mechanism of apoptosis and free radical injury after hypoxic-ischemic brain damage (HIBD) in neonatal rats. Methods: Seventy-two SD rats of 7 days old were randomly divided into 6 groups: ① normal control group; ② 0h group after HIBD; ③ 24h group after HIBD; ④ 48h after HIBD group; ② 72h after HIBD group; The rats were sacrificed at 0,24,48,72h and 7d after preparation of HIBD model. The brain was taken and the levels of superoxide dismutase (SOD) and malondialdehyde (MDA) were measured. HE and Tunel staining The apoptosis of brain cells in each group was detected. Results: After HIBD, the levels of SOD and MDA and the number of apoptotic brain cells in each group were significantly different from those in control group. There was significant difference between 48h and 72h group and other groups; there was no significant difference between 48h and 72h group Sex differences. CONCLUSION: HIBD in neonatal rats is the peak of brain injury at 48 ~ 72h. Both apoptosis and free radical injury are involved in the damage of neurons after hypoxic-ischemic insult, and the apoptosis or anti-free radical damage should be prevented within 48h get on.