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目的:探讨医用臭氧对斑马鱼幼鱼缺氧性脑损伤氧化应激过程的影响。方法:选择孵化后5天的(5pdf)野生型斑马鱼幼鱼,随机分为正常对照组(450条)、H/R组(450条,氮气法建立斑马鱼幼鱼缺氧/复氧脑损伤模型)和H/O组(450条,缺氧后臭氧水复氧,臭氧水浓度为0.1 ppm)。每组按照观测时间点不同分为3、6和12 h 3个亚组,每亚组150条。采用尼氏染色和TUNEL染色检测脑细胞凋亡情况;采用黄嘌呤氧化酶法测定超氧化物歧化酶(SOD)活力(U/ml),采用化学比色法测定丙二醛(MDA)水平(nmol/mgprot)。结果:在各时间点,H/O组脑组织凋亡细胞多于正常对照组,较H/R组少(P<0.05);H/O组脑组织SOD活性高于正常对照组及H/R组(P<0.05),H/O组脑组织MDA高于正常对照组(P<0.05),与H/R组比较差异无统计学意义(P>0.05)。结论:医用臭氧能激活缺氧后斑马鱼幼鱼脑组织抗氧化系统,减轻斑马鱼幼鱼缺氧损伤后神经细胞凋亡。
Objective: To investigate the effect of medical ozone on oxidative stress in neonatal rats with hypoxic brain injury. Methods: Five days after incubation, (5pdf) wild-type zebrafish juveniles were randomly divided into normal control group (450) and H / R group (450). The zebrafish larval hypoxia / Injury model) and H / O group (450, ozone water reoxygenation after hypoxia, ozone water concentration of 0.1 ppm). Each group was divided into 3 subgroups of 3, 6 and 12 h according to the observation time points, with 150 subgroups. The apoptosis of brain cells was detected by Nissl staining and TUNEL staining; the activity of superoxide dismutase (SOD) was measured by xanthine oxidase method; the level of malondialdehyde (MDA) was determined by chemical colorimetry nmol / mgprot). Results: At each time point, the number of apoptotic cells in brain tissue in H / O group was more than that in normal control group (P <0.05), while the activity of SOD in H / O group was higher than that in normal control group and H / (P <0.05). The content of MDA in H / O group was higher than that in normal control group (P <0.05). There was no significant difference between H / R group and H / R group (P> 0.05). Conclusion: Medical ozone can activate the antioxidant system of zebrafish juveniles after hypoxia, and reduce the apoptosis of neurons after hypoxia injury in zebrafish juveniles.