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作 者:罗璨[1] 郭莲军[1] 戴支凯[2] 吴芹[2] 石京山[2]
机构地区:[1]华中科技大学同济医学院药理学系,湖北武汉430030 [2]遵义医学院药理学教研室,贵州遵义563003
出 处:《中国药理学与毒理学杂志》2006年第1期1-6,共6页Chinese Journal of Pharmacology and Toxicology
基 金:国家自然科学基金资助项目(30171082)~~
摘 要:目的已证实牛磺酸对在体脑缺血有保护作用,本研究观察其对缺失氧糖的离体神经元是否有直接的保护作用及可能的作用机制。方法制备离体大鼠脑皮质神经元的氧糖缺失模型。在氧糖缺失前20 h及氧糖缺失4 h过程中,分别给予牛磺酸5,10和20 mmol·L-1。MTT法和流式细胞术检测神经元的死亡率;Fura-2/AM负载检测神经元内游离钙离子水平([Ca2 +]i);高效液相色谱法检测培养基中谷氨酸水平。结果氧糖缺失可致神经元死亡增加,[Ca2 +]i和培养基中谷氨酸水平异常升高;牛磺酸处理可使氧糖缺失引起的神经元死亡率明显降低,抑制氧糖缺失引起的神经元[Ca2 +]i和胞外谷氨酸浓度的异常升高。结论牛磺酸可以减轻氧糖缺失引起的大鼠皮质神经元损伤,其机制可能与其抑制胞内钙超载和抑制谷氨酸释放或漏出有关。AIM Taurine was reported neuroprotective under several ischemie models in vivo. In this study, the direct effect of taurine against oxygen-glucose deprivation (OGD) inducing acute neuronal injury and the underlying mechanisms in vitro were investigated. METHODS Four hours OGD was used to induce in vitro ischemic injury in rat cortical neurons. Taurine 5, 10 and 20 mmol· L^-1 was added 20 h before and during 4 h OGD period respectively. Mortality rate of neuron was assayed by MTT and flow cytometry methods. Level of neuronal [ Ca^2 + ] i was detected by Fura 2/AM loading. Amino acid concentrations in culture media were measured by high perfbnnance liquid chromatography. RESULTS Under OGD conditions, neuronal death was markedly increased, and the levels of neuronal [ Ca^2 + ]i and extracellular glutamate level were enhanced obviously. Taurine pretreatment obviously deceased the percentage of neuronal death induced by OGD. In addition, abnormal elevation of neuronal [ Ca^2+ ], and extracellular glutamate level induced by OGD both were markedly repressed by taufine. CONCLUSION Taurine can alleviate rat cortical nero-on injury induced by OGD, the mechanisms were likely due to repressing calcium overload and inhibiting excessive release or leakage of glutamate under such conditions.
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