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目的观察谷氨酸转运体在鱼藤酮神经毒性中的作用。方法建立星形胶质细胞与大鼠嗜铬细胞瘤(PC12)细胞共培养鱼藤酮染毒模型,并用谷氨酸转运体-1(GLT-1)和谷氨酸/天冬氨酸转运体(GLAST)特异性抑制剂二氢卡因酸盐(DHK)、L-反式吡咯烷-2,4-二羧酸(PDC)预处理。高效液相色谱(HPLC)荧光法检测星形胶质细胞胞外谷氨酸(Glu)浓度,同位素标记法检测Glu摄取能力。结果 DHK预处理组星形胶质细胞Glu摄取能力与单纯鱼藤酮中毒组比较差异无统计学意义,而PDC预处理组星形胶质细胞Glu摄取能力明显下降,胞外Glu浓度升高,与单纯鱼藤酮中毒组比较具有显著的统计学意义。结论谷氨酸转运体GLAST可能在鱼藤酮诱导的兴奋性损伤机制中起主要作用。
Objective To investigate the role of glutamate transporters in neurotoxicity of rotenone. Methods The rotenone-induced model of astrocyte co-culture with rat pheochromocytoma (PC12) cells was established. The glutamate transporter-1 (GLT-1) and glutamate / aspartate transporter GLAST) specific inhibitors dihydrocarboxylate (DHK), L-trans-pyrrolidine-2,4-dicarboxylic acid (PDC) pretreatment. The concentration of extracellular glutamate (Glu) in astrocytes was detected by high performance liquid chromatography (HPLC), and the uptake of Glu was measured by isotope labeling. Results Glu uptake capacity of astrocytes in DHK pretreatment group was not significantly different from that of rotenone poisoning group, while the Glu uptake capacity of astrocytes in PDC pretreated group was significantly decreased and the concentration of extracellular Glu increased, Rotenone poisoning group has significant statistical significance. Conclusion Glutamate transporter GLAST may play a major role in the mechanism of rotenone induced excitotoxicity.