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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。
Objectives It has been confirmed that taurine has a protective effect on cerebral ischemia in vivo. This study was to observe whether it has a direct protective effect on the exogenous neurons lacking oxygen sugar and its possible mechanism. Methods Oxygose and glucose deprivation models of isolated rat cortical neurons were established. Taurine was administered at 5, 10 and 20 mmol·L-1, respectively, 20 h before oxygen glucose deprivation and 4 h after oxygen glucose deprivation. MTT assay and flow cytometry were used to detect the neuronal death rate. Fura-2 / AM was used to detect the level of intracellular free calcium ([Ca2 +] i) in the neurons. The glutamate level in the medium was detected by high performance liquid chromatography. Results Oxygen deficiency caused an increase in death of neurons, an abnormal increase of [Ca2 +] i and glutamate levels in the culture medium. Taurine treatment significantly reduced the neuronal death rate induced by oxygen glucose deprivation and inhibited the oxygen glucose loss Of neurons [Ca2 +] i and abnormally elevated concentrations of extracellular glutamate. Conclusion Taurine can reduce the damage of cortical neurons caused by oxygen sugar deficiency in rats. The mechanism may be related to the inhibition of intracellular calcium overload and the inhibition of glutamate release or leakage.