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15-脱氧前列腺素J2在大鼠缺氧性神经细胞损伤中的作用 被引量:1

Role of 15-Deoxy-delta12,14-prostaglandin J2 in injury induced by hypoxia/reoxygenation in cultured rat cortical neurons
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摘要 目的观察环氧合酶-2的代谢产物15-脱氧前列腺素J2(15d-PGJ2)在原代培养的大鼠皮质神经细胞损伤中的作用。方法原代培养大鼠皮质神经细胞,随机分为未处理组、缺氧再复氧组、不同浓度15d-PGJ2处理的缺氧再复氧组。用噻唑蓝(MTT)比色法测定神经细胞生存率,用DNA凝胶电泳法检测神经细胞凋亡情况。结果 15d-PGJ2具有剂量依赖性保护神经细胞免于缺氧导致的死亡的作用,15d-PGJ2在10μmmol/L以上保护神经细胞,与未处理组比较差异有统计学意义(P<0.01);15d-PGJ2预处理组皮质神经细胞凋亡的DNA所出现的梯形裂解条带比单纯缺氧再复氧组明显减轻。结论环氧合酶-2代谢产物15d-PGJ2参与了神经细胞死亡、凋亡的病理过程,减轻缺氧再复氧后神经细胞的损伤。 Objective To observe the role of 15-Deoxy-delta12,14-prostaglandin J2(15d-PGJ2) in injury induced by hypoxia/reoxygenation in cultured rat cortical neurons.Methods Primary rat cortical neuron cells were cultured.Experiments include control group,hypoxia/reoxygenation group,hypoxia/reoxygenation with different dose of 15d-PGJ2(1,5,10,25,50)μmmol/L group.Cell viability was surveyed by MTT assay.Apoptosis were measured by DNA agarose electrophoresis.Results 15d-PGJ2 dose-dependently protected neuronal cell from death induced by hypoxia in vitro(P0.01).Agarose electrophoresis of the extracted DNA showed that hypoxia induced obvious DNA fragmentation,a hallmark of apoptosis,compared the group of pre-treated with 15d-PGJ2.Conclusion 15d-PGJ2 is involved in the pathogenesis of neuron death induced by hypoxia/ reoxygenation.
出处 《重庆医学》 CAS CSCD 北大核心 2010年第14期1829-1831,共3页 Chongqing medicine
基金 国家自然科学基金资助项目(30670728) 黑龙江省科技计划-国际科技合作资助项目(WB06c03) 黑龙江省卫生厅科研课题资助项目(2007-296) 哈尔滨医科大学附属第二临床医学院青年基金资助项目(QN2007-11)
关键词 大鼠 缺氧损伤 原代神经元细胞 15脱氧前列腺素J2 rats hypoxia primary neurons 15-Deoxy-delta12 14-prostaglandin J2
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