摘要
目的 探讨胆红素神经毒性脑组织细胞内 Ca2 + 变化 ,以及兴奋性氨基酸受体拮抗剂的治疗作用。 方法 在制作胆红素脑病动物模型 (新生 SD鼠 )基础上 ,通过兴奋性氨基酸受体拮抗剂磷酸甲基谷氨酰氨酸 (GAPA) 10 μg/ g干预 ,取脑组织消化、分离、漂洗、制作神经细胞悬液 ,2 -苯丙呋喃基 - 5 -恶唑羧酸五钾 /细胞膜粘合剂负载 ,荧光图像分析测定细胞内 Ca2 + 荧光强度。 结果 模型组神经细胞内 Ca2 + 荧光强度 F340 nm/ F380 nm比值为 0 .71± 0 .0 9,显著高于正常对照组的 0 .6 1±0 .0 9;干预组神经细胞内 Ca2 + 荧光强度 F340 nm/ F380 nm比值为 0 .6 5± 0 .0 8,显著低于模型组。 结论 胆红素神经毒性脑组织细胞内 Ca2 + 超载 ,兴奋性氨基酸受体拮抗剂 GAPA可拮抗胆红素毒性脑组织细胞内 Ca2 + 超载。
Objective Study the effect of NMDA receptor antagonist GAPA on the [Ca 2+ ]i of the bilirubin precipitated brain tissue. Methods 10 ug/g of GAPA was administrated peritoneally to Gunn rat with bilirubin induced encephalopathy, brain tissue suspensions was prepared, Fura 2/AM was loaded. the neural cytosolic Ca 2+ was measured by flurescence imaging analysis. Results The concentration of neural cytosolic Ca 2+ in bilirubin precipitated brain tissue was significantly more than that in the control group; NMDA receptor antagonist GAPA could significantly decrease the cytosolic Ca 2+ overload. Conclusion Cytosolic Ca 2+ overload was found in the bilirubin precipitated brain tissue. NMDA receptor antagonist GAPA could prevent the cytosolic Ca 2+ overload in bilirubin induced brain tissue.
出处
《中华围产医学杂志》
CAS
2001年第2期115-117,共3页
Chinese Journal of Perinatal Medicine
基金
上海科学技术发展基金项目 (95 41190 2 5 )