摘要
目的探讨大鼠急性脑损伤后神经书苷脂Monosialotetrahexosylganglioside（GMI）对谷氨酸受体活性变化的作用。方法采用成年雄性Wistar大鼠左颅顶液压冲击伤模型，受体放射配基结合分析法（RBA）测量双侧海马谷氨酸受体（GluR）活性，干-湿重法测量双侧脑组织水含量。结果大鼠脑损伤后GMI能显著降低伤后脑水含量的升高；抑制伤后早期GluR的最大结合量（Bmax）的增高和平衡解离常数（KD）降低，后期未发生Bmax降低和KD升高，与伤前水平基本相同；且假损伤动物GM1组与对照组或生理盐水组间GluR活性的比较，无显著差异（P＞0．05）。结论早期应用GMI能有效地拮抗GluR滥用性激活导致的兴奋性毒性，从而有效阻止脑水肿以及继发性脑损伤的发生，同时GM1对正常脑组织中GluR的活性无影响，因此具有临床应用价值。
Objective To investigate the effect of ganglioside GM1 on changes of Glutamate receptors following the fluid percussive brain injury (FPBI) in rat. Methods Adultmale Wistar rats(200±50g) were used, both the activity of glutamate receptor (GluR)in the bilateral hipocampus and the water content of brain tissue were measured following the left moderate vertex FPBI by the radioligand binding assay (RBA) and drying and wet methods separtely. Results GM1 could significantly reduce the increase of water content,control the increase of maxiimal binding capacity (Bmax) of GluR and decrease of epuilibrium dissociation constant (KD) in the prophase after injury. It could not be observed the decrease of Bmax and the increase of KD in the anaphase after injury, instead they kept at the same level as control level. It was further observed that there was no significantly difference in the sham-injury GM1treated group compared with the control group and saline-treated group sham-injury group(P>0.05). Conclusion Early adoption of GM1 could effectively resist the abusive glutamate receptor stimulation induced excitotoxicity, and then prevent the occurrence of the brain edema and secondary brain injury. GM1 has no infiuence to the activity of GluR in normal brain tissue, hence, it has clinical value.
出处
《创伤外科杂志》
1999年第4期221-224,共4页
Journal of Traumatic Surgery
关键词
GM1
脑损伤
谷氨酸受体
GM1 Brain injury Glutamate receptor Rat
