机构地区:[1]徐州医学院附属医院新生儿科,221002 [2]徐州医学院附属医院中医科,221002
出 处:《中华医学杂志》2009年第16期1144-1147,共4页National Medical Journal of China
基 金:江苏省卫生厅医学科技发展基金(Z200308);徐州市科学技术项目(200310)
摘 要:目的研究缺氧缺血性脑损伤(HIBD)新生大鼠脑组织低氧诱导因子1α(HIF-1α)mRNA的表达及参麦注射液的干预作用。方法新生7d龄SD大鼠随机分为假手术组、生理盐水组、参麦组,又各分为缺血缺氧后2、12、24h,3、7、14d6个亚组,每亚组9只。采用反转录(RT)-PCR法检测鼠脑HIF-1α mRNA;流式细胞仪膜联蛋白V/碘化丙啶双染色法检测细胞凋亡。结果(1)缺氧缺血后2h,生理盐水组和参麦组右侧海马神经元凋亡率即均高于假手术组(均P〈0.05),于24h达到峰值后开始下降[(16.80±1.44)%、(11.95±1.13)%],14d各组差异均无统计学意义(均P〉0.05)。参麦组海马神经元凋亡率在缺血缺氧后12、24h,3和7d均明显低于生理盐水组(均P〈0.05)。(2)缺血缺氧后2h生理盐水组、参麦组新生大鼠右侧大脑中HIF—1α mRNA的表达即均高于假手术组(均P〈0.05),于24h达峰值后开始下降[(44.32±4.03)%、(35.63±3.73)%],14d各组表达差异均无统计学意义(均P〉0.05);参麦组大脑中HIF-1α mRNA的表达在缺血缺氧后12、24h,3和7d均明显高于生理盐水组(均P〈0.05)。结论新生大鼠HIBD时HIF-1α mRNA表达增强,参麦注射液可提高新生大鼠HIBD后的HIF—1αmRNA的表达,减少新生大鼠缺氧缺血后神经元凋亡的发生。Objective To investigate the effects of Shemnai injection containing active principles of Ginseng and ophiopogon root on the expression of hypoxia-inducible factor 1-α (HIF-1α) in brain after hypoxic-ischemic brain damage (HIBD) . Methods 108 neonatal SD rats were randomly divided into 2 equal groups: (~) Shenmai group (Group SM), undergoing ligation of the right common carotid artery to establish HIBD models, breathing immediately a mixed gas with 8% oxygen and 92% nitrogen for 2 h to cause HI insult, and then injected intraperitoneally with Shenmai injection 10 mg/kg once a day for 7 d, and ~) normal saline group (Group NS) undergoing ligation of the right common carotid artery to establish HIBD models, breathing immediately a mixed gas with 8% oxygen and 92% nitrogen for 2 h, and then injected intraperitoneally with NS 10 mg/kg once a day for 7 d. Another 54 neonatal rats underwent sham operation but did not undergo hypoxia as control group (Group C), 2, 12, and 24 h, and 3, 7, and 14 d after HI insult 9 rats from each group were killed with their right hippocampal tissues taken out. Flow cytometry was used to examine the apoptotic rate of the hippocampal neurons. RT-PCR was used to detect the mRNA expression of HIF-1α. Results ( 1 ) The apoptosis rate of the right hippocampal tissues began increase 2 h after HI insult, peaked 24 h after HI, then gradually decreased, and almost returned to the original levels 14 d after HI. There was no significant differences in apoptosis rates 14 d after HI among the 3 groups ( all P 〉 0. 05). The neuron apoptosis rates 12 h, 24 h, 3 d, and 7 d after HI of Group SM were all significantly lower than those of Group NS ( e. g 24 h: ( 11.95 ± 1.13 ) % vs ( 16. 80 ± 1.44) %, all P 〈 0. 05 ). (2) The HIF-1α mRNA expression level in right brain began to increase 2 h after HI, peaked 24 h after HI, then gradually decreases, and returned to the original level 14 d after HI in both Group SM and Group NS; the HIF-1α mRNA
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