灵芝多糖对癫痫大鼠脑中谷氨酸转运体的影响

摘要

objective To observe and investigate the influence of ganoderma lucidum polysaccharide on GLAST, GLT-1 and EAAC1 in the cortex and hippocampus of epileptic rat. Study on the pathogenesis of epilepsy and the mechanism of action of ganoderma lucidum polysaccharide. Methods The 32 SD rats were randomly divided into normal control group,epilepsy model group,ganoderma lucidum polysaccharides and carbamazepine group,each group of eight. The rats of epilepsy model group,ganoderma lucidum polysaccharides and carbamazepine group made by intraperitoneal injection of pentetrazole(PTZ). After the experiment,get the rats brain tissue quickly. Using im-munohistochemical and colorimetry to detect the index changes of cortex and hippocampus. Results GLAST1,GLT1, EAAC1 in the brain of epileptic rat lower in epilepsy model group than the normal control group:cortex(31. 87 ± 4. 76),( 48. 00 ± 5. 34),(42. 87 ± 4. 01),(52. 12 ± 3. 75),(40. 25 ± 2. 81),(46. 87 ± 3. 04);hippocampus (29. 87 ± 4. 32),(44. 51 ± 4. 81),(36. 50 ± 3. 02),(47. 00 ± 3. 20),(35. 62 ± 3. 42),(42. 12 ± 3. 56);GLAST, GLT-1,EAAC1 in the brain of epileptic rat higher in ganoderma lucidum polysaccharides group and carbamazepine group than the epilepsy model group:cortex(40. 50 ± 4. 47),(31. 87 ± 4. 76),(48. 87 ± 3. 48),(42. 87 ± 4. 01), (43. 87 ± 2. 53),(40. 25 ± 2. 81);hippocampus(37. 75 ± 3. 61),(29. 87 ± 4. 32),( 41. 25 ± 2. 60),(36. 50 ± 3. 02),(39. 50 ± 2. 61),(35. 62 ± 3. 42);GLAST1,GLT1,EAAC1 were no significant differences in ganoderma lu-cidum polysacchairides group and carbamazepine group. Conclusion Ganoderma lucidum polysaccharide can in-crease the GLAST,GLT-1 and EAAC1 in the epileptic rats brain tissue,speed up the process of eliminating glutamic acid.%目的：观察和探讨灵芝多糖干预后戊四氮（ PTZ）致痫大鼠皮质和海马区兴奋性谷氨酸转运体（EAAT）GLAST（EAAT1）、GLT1（EAAT2）、EAAC1（EAAT3）的变化，进一步研究癫痫的发病机制及灵芝多糖的作用机制。方法 SD 大鼠32只，随机分为正常对照组、癫痫模型组、灵芝多糖组和卡马西平组，每组8只。癫痫组、灵芝多糖组和卡马西平组采用 PTZ 腹腔注射制作慢性癫痫点燃模型。实验结束后断头迅速取脑，采用免疫组化法检测皮质和海马区各指标的变化。结果癫痫模型组大鼠脑中 GLAST、GLT1、EAAC1的表达较正常对照组降低：皮质（31.87±4.76）、（48.00±5.34），（42.87±4.01）、（52.12±3.75），（40.25±2.81）、（46.87±3.04）；海马：（29.87±4.32）、（44.51±4.81），（36.50±3.02）、（47.00±3.20），（35.62±3.42）、（42.12±3.56）；灵芝多糖和卡马西平组大鼠脑中 GLAST1、GLT1、EAAC1的表达较癫痫模型组升高：皮质（40.50±4.47）、（31.87±4.76），（48.87±3.48）、（42.87±4.01），（43.87±2.53）、（40.25±2.81）；海马：（37.75±3.61）、（29.87±4.32），（41.25±2.60）、（36.50±3.02），（39.50±2.61）、（35.62±3.42）。灵芝多糖组和卡马西平组之间 GLAST1、GLT1、EAAC1三者的表达无统计学意义。结论灵芝多糖能够升高癫痫大鼠脑中 GLAST、GLT1、EAAC1的表达，加速了兴奋性氨基酸 Glu（谷氨酸）的清除。降低神经元兴奋性、减少神经系统损伤而抑制癫痫的发作。