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研究高糖对神经元缺氧的影响 ,并探讨其钙相关机制。利用 SD大鼠大脑皮质神经元体外缺氧模型 ,通过对细胞活力的检测 ,观察浓度分别为 2 2 .7(对照组 ) ,30 ,40 ,50 ,60 (高糖组 ) mmol/ L的葡萄糖对神经元缺氧的影响 ;以 Fura- 2 / Am为荧光指示剂 ,测定细胞内游离钙离子浓度 ([Ca2 +]i。结果发现当培养基中葡萄糖浓度达到 60 mmol/ L时 ,高糖可引起缺氧神经元损伤 ;与对照组相比 ,有钙介质与无钙介质中静息[Ca2 +]i 均升高 ,P<0 .0 1 ;但对照组与高糖组在有钙介质中对氯化钾 (KCl)、谷氨酸 (Glu)刺激引起的[Ca2 +]i 升高无明显差异 ,P>0 .0 5;在无钙介质中 ,对氯化钙 (Ca Cl2 )引起的 [Ca2 +]i 增高率无明显差别 ,P>0 .0 5。本研究表明 :高糖对神经元的损伤作用可能与其促进细胞内钙离子释放 ,诱发细胞内钙超载有关
To study the effect of high glucose on neuronal hypoxia and to explore its calcium-related mechanism. The hypoxia model of cerebral cortical neurons in SD rats was used to detect the viability of cells in vitro. The concentrations of glucose (mmol / L, 30, 40, 50, 60 mmol / L) On the neuronal hypoxia. The intracellular free calcium concentration ([Ca2 +] i) was measured with Fura-2 / Am as fluorescent indicator. The results showed that when the glucose concentration in the medium reached 60 mmol / L, Compared with the control group, resting [Ca2 +] i in both calcium and calcium-free medium increased, P <0.01; however, in control group and high glucose group, calcium There was no significant difference in the increase of [Ca2 +] i induced by potassium chloride (KCl) and glutamic acid (Glu) in the medium, P> 0.05. In medium without CaCl2 ) Caused by [Ca2 +] i increased rate no significant difference, P> 0 .0 5. This study shows that: the role of high glucose on neurons damage may be related to its promotion of intracellular calcium release, induced by intracellular calcium overload