中文摘要：

目的观察神经节苷脂（GM1）对脑外伤大鼠大脑皮质和海马区神经生长相关蛋白-43（GAP-43）表达的影响,探讨GM1促进脑外伤神经修复的可能机制。方法选择出生10周雄性SD大鼠200只,随机分为假手术组60只,无脑外伤,术前腹腔注射生理盐水3 d。脑外伤模型140只,分为模型组70只,术前腹腔注射生理盐水3 d;GM1组70只,术前腹腔注射GM13 d。应用酶联免疫法检测大鼠大脑顶叶皮质和海马区GAP-43于0～24 h不同时间点的表达情况,并在术后1～5 d不同时间点进行行为学检测。结果 （1）GM1组大鼠大脑顶叶皮质0～16 h和海马区0～24 h GAP-43的表达均明显低于模型组（P〈0.01）,而与假手术组比较,大鼠顶叶皮质区8～24 h GAP-43的表达,差异有统计学意义（P〈0.01）。（2）GM1组大鼠大脑顶叶皮质GAP-43的表达,术后随着时间的增加而升高,至24 h已达模型组水平。（3）假手术组的行为学表现1～5 d均优于模型组和GM1组（P〈0.01）,GM1组在术后2～5 d运动能力逐步增强,行为学表现优于模型组（P〈0.05）。结论预防性使用GM1有效地促进大鼠大脑皮质GAP-43的表达升高,降低脑外伤大鼠脑损伤程度,从而发挥其对实验性脑外伤大鼠的神经保护作用。

英文摘要：

Objective To observe the effects of the ganglioside（GM1） on brain trauma cerebral cortex and hippocampus nerve growth associated protein（GAP-43） expression in rats, to explore the possible mechanisms of GM1 promoting the nerve repair of traumatic brain injury. Methods200 male SD rats（10 weeks old）, were used in this experiment. Of which 60 mice were randomly divided into sham group, no brain trauma, preoperative intraperitoneal injection of saline3 d. 140 mice were used as traumatic brain injury model, divided into model group 70 mice,preoperative intraperitoneal injection of saline 3 d; GM1 group 70 mice, preoperative intraperitoneal injection GM13 d. ELISA was used to detect parietal cerebral cortex and hippocampus of GAP-43 expression at 0～24 h at different time, and after 1～5 d at different time take the behavioral testing. Results（1） 0～16 h GAP-43 expression in rat brain GM1 parietal cortex and 0～24 h hippocampus were significantly lower than the model group（P〈0.01）, and compared with the sham group, there was no significant difference（P〉0.01）.（2） GM1 rat parietal cortex GAP-43 expression, postoperative increase over time and reached the level of the untreated group at 24 h.（3） Conducts in sham group 1～5 d school performance was better than these in model group and GM1 group（P〈0.01）, GM1 group gradual increase in exercise capacity after 2～5 d, behavioral performance was better than that in the model group（P〈0.05）. Conclusions Prophylactic use of GM1 can effectively promote brain cortex GAP-43 expression and reduce the extent of brain damage in rats with traumatic brain injury, which plays its neuroprotection roles in experimental traumatic brain injury in rats.