论文部分内容阅读
目的和方法 :采用核团微量注射、光化学分析等实验方法 ,观察大鼠脑内SOD和MDA在CCK 8调节癫痫发作中的变化。结果 :①与正常大鼠比较 ,遗传性听源性癫痫易感大鼠皮层、海马、下丘脑及垂体内SOD活性、MDA含量无显著差异 (P >0 .0 5 ) ;②大鼠癫痫发作后 ,上述区域内SOD活性明显降低 (P <0 .0 5 ) ,而MDA含量明显增加 (P <0 .0 5 ) ,若癫痫发作次数增加 ,该变化愈显著 (P <0 .0 1) ;③大鼠海马CA3 区注射CCK 8后 ,皮层、海马、下丘脑及垂体内SOD活性及MDA含量无明显改变 (P >0 .0 5 )。诱发癫痫时 ,在癫痫发作减弱的同时 ,上述区域内SOD活性显著增高 (P <0 .0 1) ,MDA含量显著降低 (P <0 .0 5 )。结论 :癫痫发作后 ,脑内神经元抗氧化能力降低 ,CCK 8可压抑癫痫发作 ,提高脑内神经元的抗氧化能力。
PURPOSE AND METHODS: The nucleus microinjection and photochemical analysis were used to observe the changes of SOD and MDA in the brain of CCK 8-induced seizures. Results: ①Compared with normal rats, there was no significant difference in SOD activity and MDA content between cortex, hippocampus, hypothalamus and pituitary in hereditary auditory epilepsy rats (P> 0.05); ②Patients with epilepsy (P <0.05), while the content of MDA increased significantly (P <0.05). If the number of epileptic seizures increased, the change was more significant (P <0.01) ; ③ After injection of CCK 8 into CA3 area of hippocampus, there was no significant change in SOD activity and MDA content in cortex, hippocampus, hypothalamus and pituitary (P> 0.05). When epilepsy was induced, the activity of SOD in the above regions was significantly increased (P <0.01) and the content of MDA was significantly decreased (P <0.05), while the seizures decreased. Conclusion: After epileptic seizures, the ability of anti-oxidation of neurons in the brain is reduced. CCK 8 can suppress seizures and improve the antioxidant capacity of neurons in the brain.