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目的观察托吡酯(TPM)对戊四氮(PTZ)所致慢性癫痫大鼠癫痫发作及神经细胞凋亡的影响,以为其作为神经细胞保护剂使用提供理论依据。方法建立癫痫大鼠模型(模型组)和建立癫痫大鼠模型后以TPM进行干预(TPM预防组),并以腹腔注射生理盐水作为对照组,分别进行动物行为学观察及检测各组神经细胞凋亡和caspase-3阳性神经细胞。结果TPM预防组痫性发作级别较模型组显著降低,惊厥潜伏期较模型组明显延长,差异均有统计学意义(分别P<0.01和<0.05),惊厥持续时间两组差异无统计学意义(P>0.05);模型组神经细胞凋亡数、caspase-3阳性神经细胞数较TPM预防组、对照组显著增加,TPM预防组神经细胞凋亡数、caspase-3阳性神经细胞数较对照组显著增加,差异均有高度统计学意义(均P<0.01)。结论TPM对PTZ所致慢性癫痫大鼠模型有预防作用;TPM能有效控制PTZ所致慢性癫痫大鼠脑组织海马区神经细胞凋亡,其可能机制是降低caspase-3的表达,从而发挥脑保护作用。
Objective To investigate the effects of topiramate (TPM) on the seizure and neuronal apoptosis in chronic epileptic rats induced by pentylenetetrazole (PTZ), and to provide a theoretical basis for its use as a neuroprotective agent. Methods The epilepsy rat model (model group) and the epilepsy rat model were established and treated with TPM (TPM prophylaxis group). The animals were injected intraperitoneally with normal saline as the control group, respectively. Death and caspase-3 positive neurons. Results The level of seizure in the TPM prevention group was significantly lower than that in the model group, and the latent period of convulsion was significantly longer than that in the model group (P <0.01 and <0.05, respectively). There was no significant difference in the duration of seizure between the two groups (P > 0.05). The number of apoptotic neurons and the number of caspase-3 positive neurons in the model group were significantly higher than those in the TPM prevention group and the control group. The number of apoptotic neurons and the number of caspase-3 positive neurons in the TPM prevention group were significantly higher than those in the control group , The differences were highly statistically significant (all P <0.01). Conclusion TPM can prevent PTZ-induced chronic epilepsy rat model. TPM can effectively control the apoptosis of hippocampal neurons in PTZ-induced chronic epileptic rat brain. Its possible mechanism is to decrease the expression of caspase-3 and to protect the brain effect.