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目的:观察去铁敏对谷氨酸所致星型胶质细胞损伤的保护作用。方法:建立原代培养的星型胶质细胞谷氨酸毒性模型,采用免疫组化、Hoechst染色检测细胞形态及核固缩情况。CCK-8法检测细胞活力。生化法检测羟自由基、MDA变化。用显微荧光测量技术监测神经元内钙信号的动态变化。结果:随着谷氨酸浓度的增加细胞损伤也逐渐加重。与对照组相比,去铁敏处理后细胞对0.5,1.0,5.0mmol/L谷氨酸损伤形态保持良好;细胞核固缩率减少,分别为(10.44±5.03)%,(7.93±5.04)%和(11.01±3.73)%(P<0.05);细胞活力下降减轻,分别为(94.72±2.20)%(P<0.05),(82.49±1.94)%和(67.94±5.55)%(P<0.01)。去铁敏处理后羟自由基水平下降,为10.17±1.79(P<0.01)。MDA水平下降,为7.36±1.47(P<0.01)。去铁敏预处理后钙离子增高的幅度及出现钙离子变化的细胞数较对照有明显减少。结论:去铁敏能减轻谷氨酸导致的星型胶质细胞损伤,能减少谷氨酸导致的星型胶质细胞内钙浓度的升高及自由基水平,这可能是去铁敏保护作用的机理之一。
Objective: To observe the protective effect of deferoxamine against astrocyte injury induced by glutamate. Methods: Primary cultured astrocyte glutamate toxicity model was established. Immunohistochemistry and Hoechst staining were used to detect cell morphology and nuclear condensation. CCK-8 method to detect cell viability. Biochemical detection of hydroxyl radical, MDA changes. Monitoring the Dynamic Changes of Calcium Signals in Neurons by Microfluorescence Measurement. Results: As the glutamate concentration increased, cell injury also gradually increased. Compared with the control group, the cells treated with deferoxamine maintained good morphology of glutamate at 0.5, 1.0 and 5.0 mmol / L, and the nuclear shrinkage rate decreased by (10.44 ± 5.03)% and (7.93 ± 5.04)%, respectively (94.72 ± 2.20)% (P <0.05), (82.49 ± 1.94)% and (67.94 ± 5.55)%, respectively (P <0.01) and (11.01 ± 3.73)% . After deferoxamine treatment, the level of hydroxyl radical decreased to 10.17 ± 1.79 (P <0.01). MDA levels decreased to 7.36 ± 1.47 (P <0.01). Deferoxamine pretreatment after the increase in the magnitude of calcium and calcium changes in the number of cells than the control significantly reduced. Conclusion: deferoxamine can reduce glutamate-induced astrocyte injury, reduce glutamate-induced astrocyte intracellular calcium concentration and free radical levels, which may be deferoxamine protective effect One of the mechanisms.