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作 者:张巍[1] 阴怀清[2] 张新[2] 栗红[2] 张晓佳[2] 李迎敏[2] 冯钰淑
机构地区:[1]山西医科大学,在读硕士太原030001 [2]山西医科大学第一医院,太原030001
出 处:《中西医结合心脑血管病杂志》2014年第12期1540-1542,共3页Chinese Journal of Integrative Medicine on Cardio-Cerebrovascular Disease
基 金:山西省回国留学人员科技基金资助项目(No.2011-095);山西省卫生厅科技攻关基金项目(No.2011-018)
摘 要:目的探讨亚低温干预下新生大鼠缺氧缺血性脑损伤(HIBD)时环氧化酶2(COX-2)基因表达变化及意义。方法 120只7 d龄SD大鼠,采用Rice法建立新生大鼠缺氧缺血脑损伤模型,随机分为假手术组、常温组、亚低温组,每组又根据处死时间的不同分为1 h、6 h、12 h、24 h、48 h五个亚组,用实时荧光定量聚合酶链反应检测新生大鼠COX-2m RNA表达。结果假手术组COX-2m RNA表达甚微,且各组之间无明显变化;常温组COX-2m RNA表达6 h开始上调且逐渐增加,24 h含量达高峰,24 h^48h维持在高峰(P<0.05);亚低温组各组COX-2m RNA表达与常温组各时间点比较均降低(P<0.05)。结论 COX-2在新生大鼠HIBD形成中发挥一定的作用,亚低温干预能降低HIBD后不同时间脑组织COX-2的表达活性,提示在恰当的时间窗内进行亚低温干预治疗对脑保护是有效的。Objective To observe the changes of cycloxygenase 2(COX 2)gene expression in brain tissue after hypoxia is-chemia brain damage (HIBD)and receiving mild hypothermia intervention.Methods One hundred and twenty seven day old neo-natal Sprague Dawley(SD)rats that adopted Rice method to establish the model of HIBD and were randomly divided into three groups:Sham operated group (n= 40),normal temperature group (n= 40)and mild hypothermia (n= 40)group.The experimen-tal groups were further divided into five sub groups (n= 8 in each group)based on different time points after HIBD (1 h,6 h,12 h, 24 h,48 h)respectively.Fluorescence quantitative PCR (PT PCR)technique was used to determine the expression changes of COX 2 mRNA in brain tissues.Results COX 2 mRNA expressed had no significant change in sham operated group.The expres-sion of normal temperature group increased at 6 h after HIBD,24 h to the peak level,24 h to 48 h gradual y increased(P〈0.05).The COX 2 mRNA expression in mild hypothermia group was significantly lower than that in HIBD group at each time points (P〈0.05). Conclusion COX 2 participated in HIBD of neonatal rats.Mild hypothermia intervention could reduce the expression of COX 2 mRNA in brain tissue after HIBD.Therefore,mild hypothermia intervention at the appropriate time window had some cerebral protec-tion effects on the brain tissues of neonatal rats after HIBD.
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