红藻氨酸致痫后大鼠海马ERK、P38 MAPK和JNK的活性变化

目的研究红藻氨酸(KA)诱导大鼠癫痫发作后海马组织细胞外调节蛋白激酶(ERK)、p38MAPK和c-jun氨基末端激酶(JNK)的活性(磷酸化状态)的变化情况。方法立体定向大鼠侧脑室内注射KA引起大鼠癫痫发作,采用Western-blot方法观察KA致痫后大鼠海马中活性ERK、p38MAPK和JNK的变化。结果KA诱导大鼠癫痫发作后,海马组织ERK、p38MAPK和JNK的磷酸化水平开始增高,分别于30min、1h和30min后达高峰,呈对照组的4.76倍、2.16倍和3.95倍,两组比较差异具有显著性(P<0.01),之后逐渐下降。结论KA致痫大鼠癫痫发作后,海马组织MAPKs的活性产生变化,其信号通路可能参与癫痫发作后海马组织的病理生理反应过程。

Change of MAPKs activation in rat hippocampus following kainic acid-induced epileptic seizures

Objective To investigate the change of the activations of ERK, p38 MAPK, and JNK in rat hippocampus after a unilateral stereotaxic microinjection of KA into the lateral ventricle of rats with kainic acid (KA)-induced epileptic seizure. Methods By means of western-blotting, the activations of those kinases were observed at different time points after a unilateral stereotaxic microinjection of KA into the lateral ventricle of rats, which caused limbic and generalized convulsive seizures. Results The activations of ERK, p38 MAPK, and JNK began to increase after epileptic seizure and reached the peak at 30 min, 1 h, and 30 min, respectively. And their activations were 4.76-fold (P<0.01), 2.16-fold (P<0.01), and 3.95-fold (P<0.01) compared with the average activations in control rats, respectively. Then they began to ebb. Conclusion Following KA-induced seizure, the activations of ERK, p38 MAPK, and JNK in rat hippocampus change at different temporal pattern. There is a probability that MAPKs signal pathway is involved in the process of pathologic and physiologic reaction in rat hippocampus following KA-induced epileptic seizure.