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机构地区:[1]苏州大学附属儿童医院儿科医学研究所小儿神经实验室,江苏苏州215003
出 处:《实用儿科临床杂志》2010年第2期116-117,150,共3页Journal of Applied Clinical Pediatrics
摘 要:目的探讨可塑性相关基因-1(PRG-1)在反复惊厥新生大鼠大脑皮质中的动态表达。方法出生6d(P6)的SD大鼠48只随机分成2组,每组各24只。实验组在P6时吸入三氟乙醚诱导惊厥发作,持续30min,连续6d;对照组同样操作但不吸入三氟乙醚。于最后1次惊厥1.5h、6.0h、24.0h、7d,取其大脑皮质,并在每个时间点设未行任何干预的对照组。用免疫印迹方法检测各组新生大鼠大脑皮质中PRG-1蛋白的表达。采用SPSS17.0软件进行统计学处理。结果对照组新生大鼠4个时间点间大脑皮质PRG-1的表达无统计学差异(F=2.044,P=0.140),实验组各时间点之间大脑皮质PRG-1的表达亦无统计学差异(F=2.483,P=0.090)。1.5h、6.0h、24.0h3个时间点实验组新生大鼠大脑皮质PRG-1的表达与对照组比较均无统计学差异(t=0.295、0.627、0.934,Pa>0.05)。7d时,实验组大脑皮质PRG-1表达明显高于对照组(t=2.347,P=0.041)。结论PRG-1在新生大鼠反复长程惊厥后的远期表达增多,可能参与发育期惊厥性脑损伤的病理生理机制。Objective To explore the dynamic expression of plasticity related gene 1(PRG-1) in cerebral cortex of neonatal rats with recurrent seizures.Methods Forty-eight neonatal rats were divided into 2 groups:the experimental group(n=24) and the control group(n=24).The volatile agent flurothyl was used to induce 30 min seizure attack.At postnatal day 6(P6),recurrent seizures were induced once per day for consecutive 6 days in the experimental group.Control rats were placed into the container for an equal amount of time to their counterpart without exposure to flurothyl.At 1.5 h,6.0 h,24.0 h,7 d after the last convulsion,PRG-1 protein levels in cerebral cortex were detected by Western blotting method.SPSS 17.0 software was used to analyze the data.Results There was no significant difference of PRG-1 expression in cerebral cortex of control group among the four time points(F=2.044,P=0.140),and in the experimental group also had no significant difference(F=2.483,P=0.090).At 1.5 h,6.0 h,24.0 h,the expression of PRG-1 in cerebral cortex had not significantly different between the experimental and control groups(t=0.295,0.627,0.934,Pa〉0.05).However,the level of PRG-1 protein in cerebral cortex of experimental group was significantly higher than that of control group at 7 d(t=2.347,P=0.041).Conclusion The up-regulated expression of PRG-1 in cerebral cortex may be associated with the recurrent neonatal seizure-induced brain damage.
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