CAJ | 학술논문

目的　探讨N-甲基-D-天冬氨酸(NMDA)受体水平胆红素脑病发生机制与防治措施。方法　制作胆红素脑病动物模型基础上，在体脑内微透析提取兴奋性氨基酸(EAA)神经递质，HPLC检测天冬氨酸(Asp)、谷氨酸(Glu)、甘氨酸(Gly)，并给予模型动物NMDA受体拮抗剂GAPA干预，电镜检测脑组织超微结构，荧光检测脑组织ATP与细胞内Ca2+含量。结果　胆红素毒性脑组织ATP含量显著降低，细胞外Gly与细胞内Ca2+显著升高；GAPA不影响胆红素毒性脑组织ATP含量，但可显著降低细胞内Ca2+，减轻胆红素毒性脑水肿。结论　NMDA受体过度活化致细胞内Ca2+超载参与介导胆红素神经毒性，NMDA受体拮抗剂可望成为胆红素神经毒性防治的重要途径。
목적　탐토N-갑기-D-천동안산(NMDA)수체수평담홍소뇌병발생궤제여방치조시。방법　제작담홍소뇌병동물모형기출상，재체뇌내미투석제취흥강성안기산(EAA)신경체질，HPLC검측천동안산(Asp)、곡안산(Glu)、감안산(Gly)，병급여모형동물NMDA수체길항제GAPA간예，전경검측뇌조직초미결구，형광검측뇌조직ATP여세포내Ca2+함량。결과　담홍소독성뇌조직ATP함량현저강저，세포외Gly여세포내Ca2+현저승고；GAPA불영향담홍소독성뇌조직ATP함량，단가현저강저세포내Ca2+，감경담홍소독성뇌수종。결론　NMDA수체과도활화치세포내Ca2+초재삼여개도담홍소신경독성，NMDA수체길항제가망성위담홍소신경독성방치적중요도경。
Objective Study the NMDA receptor activity in bilirubin induced encephalopathyand its molecular mechanism. Methods On the basis of bilirubin induction and NMDA receptor an-tagonist GAPA administration in guinea pigs. The brain extracellular EAA neurotransmitter was ex-tracted with microdialysis and analysed with HPLC; then, brain tissue ATP was measured by fluores-cence assay and intracellular Ca2 + was measured by fluorescence imaging analysis. Results ATP andEAA Neurotransmitter Gly were greatly increased in the bilirubin induced neurotoxicity brain; neuralcytosolic Ca2 + in the bilirubin precipitated brain tissue was significantly more than that in the controlgroup; NMDA receptor antagonist GAPA could significantly decrease the cytosolic Ca2+ overload.Conclusion EAA neurotransmitter Gly increased the sensitivity of the ligand Asp and Glu to theNMDA receptor, thus increased the NMDA receptor activity and cytosolic Ca2 + in the bilirubin precipi-tated brain tissue. NMDA receptor antagonist GAPA could prevent the cytosolic Ca2 + overload, and re-lieve brain edema.