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目的:观察癫发作后不同时间海马组织凋亡相关蛋白表达水平的变化,探讨米诺环素(MT)减轻癫所致的海马神经元损伤的机制。方法:杏仁核立体定向注射红藻氨酸(KA)建立大鼠癫模型,随机分为治疗(MT)组和非治疗(KA)组,以杏仁核注射生理盐水为空白对照(SC)组。用免疫印迹法检测caspase-3裂解片段及Bcl-2和Bcl-xl表达水平的变化。结果:与KA组相比,MT组caspase-3裂解水平明显降低(P<0.05)并接近SC组;Bcl-2在癫发作终止后2h开始上调,24h达高峰并持续到72h。Bcl-xl上调不明显。结论:米诺环素能减少caspase-3的裂解,抑制线粒体凋亡通路激活,从而减轻癫发作对神经元的损伤。这一作用与抗凋亡因子Bcl-2的上调有关,提示Bcl-2可能是癫潜在的治疗靶点。
OBJECTIVE: To observe the changes of apoptosis-related proteins in hippocampus at different time points after epileptic seizures and to explore the mechanism of mitomycin (MT) on the neuronal damage induced by epilepsy. Methods: Rats were randomly divided into treatment (MT) group and non-treatment (KA) groups. Kainate (KA) was injected into the amygdala to establish a rat model of epilepsy by stereotactic injection of kainic acid (KA) . Western blotting was used to detect the expression of caspase-3 cleavage fragment and Bcl-2 and Bcl-xl. Results: Compared with KA group, the cleavage level of caspase-3 in MT group was significantly lower than that in SC group (P <0.05), and close to SC group. Bcl-2 began to rise at 2h after termination of epileptic seizure and peaked at 24h and reached 72h. Bcl-xl upregulation is not obvious. CONCLUSION: Minocycline can reduce the cleavage of caspase-3 and inhibit the activation of mitochondrial apoptotic pathway, thus alleviating the neuronal damage induced by epileptic seizures. This effect is related to the up-regulation of anti-apoptotic factor Bcl-2, suggesting that Bcl-2 may be a potential therapeutic target for epilepsy.