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探讨胆红素神经毒性脑组织细胞内 Ca2 +变化以及 NMDA受体拮抗剂GAPA治疗作用。方法 :制作胆红素脑病动物模型基础上予 NMDA受体拮抗剂GAPA干预后 ,消化分离漂洗制作神经细胞悬液 ,Fura- 2 /AM负载 ,荧光图像分析测定细胞内 Ca2 +。结果显示 :胆红素毒性脑组织细胞内 Ca2 +较对照组明显升高 ,NMDA受体拮抗剂 GAPA可显著减轻胆红素毒性脑组织细胞内 Ca2 +超载。因此 :胆红素神经毒性脑组织细胞内 Ca2 +超载 ,NMDA受体拮抗剂 GAPA可拮抗胆红素毒性脑组织细胞内 Ca2 +超载。
To investigate the change of intracellular Ca2 + in neurons of bilirubin neurotoxicity and the therapeutic effect of NMDA receptor antagonist GAPA. Methods: The animal model of bilirubin encephalopathy was pretreated with GAPA, an NMDA receptor antagonist. The nerve cell suspension was prepared by digestion and rinsing. Fura-2 / AM was loaded. The intracellular Ca2 + was detected by fluorescence image analysis. The results showed that the intracellular Ca2 + in bilirubin-toxic brain tissue was significantly higher than that in the control group, and the NMDA receptor antagonist GAPA significantly reduced the intracellular Ca2 + overload in the bilirubin-toxic brain tissue. Therefore: Bilirubin neurotoxicity intracellular Ca2 + overload, NMDA receptor antagonist GAPA can antagonize the bilirubin toxicity of intracellular Ca2 + overload.