冯杰, 邓子辉, 张金英, 薛辉, 梁辰, 李建华, 颜光涛. 瘦素在海人酸诱导小鼠颞叶癫痫海马损伤中的作用[J]. 解放军医学院学报, 2015, 36(4): 388-392. DOI: 10.3969/j.issn.2095-5227.2015.04.023
引用本文: 冯杰, 邓子辉, 张金英, 薛辉, 梁辰, 李建华, 颜光涛. 瘦素在海人酸诱导小鼠颞叶癫痫海马损伤中的作用[J]. 解放军医学院学报, 2015, 36(4): 388-392. DOI: 10.3969/j.issn.2095-5227.2015.04.023
FENG Jie, DENG Zihui, ZHANG Jinying, XUE Hui, LIANG Chen, LI Jianhua, YAN Guangtao. Role of leptin in kainic acid-induced hippocampal injury of temporal lobe epilepsy in mice[J]. ACADEMIC JOURNAL OF CHINESE PLA MEDICAL SCHOOL, 2015, 36(4): 388-392. DOI: 10.3969/j.issn.2095-5227.2015.04.023
Citation: FENG Jie, DENG Zihui, ZHANG Jinying, XUE Hui, LIANG Chen, LI Jianhua, YAN Guangtao. Role of leptin in kainic acid-induced hippocampal injury of temporal lobe epilepsy in mice[J]. ACADEMIC JOURNAL OF CHINESE PLA MEDICAL SCHOOL, 2015, 36(4): 388-392. DOI: 10.3969/j.issn.2095-5227.2015.04.023

瘦素在海人酸诱导小鼠颞叶癫痫海马损伤中的作用

Role of leptin in kainic acid-induced hippocampal injury of temporal lobe epilepsy in mice

  • 摘要: 目的 探讨瘦素(Leptin)与颞叶癫痫发生、发展过程的关系。 方法 外源Leptin注射C57BL/6J小鼠后,右侧海马微量注射200 ng海人酸(kainic acid,KA)诱导颞叶癫痫,记录小鼠癫痫评分,1周后观察小鼠海马病理变化,包括Western blot检测Bax的表达水平,尼式染色(Nissl staining)观察海马Hilus区神经元丢失,免疫荧光检测Hilus区星形胶质细胞活化与增殖。 结果 在200 ng KA诱导的颞叶癫痫模型基础上,10 mg/kg外源Leptin预处理后,癫痫评分增加约52%,Bax表达水平升高约75%(P< 0.05),海马Hilus区神经元丢失严重,星形胶质细胞过度活化。 结论 Leptin增加了KA诱导的神经元凋亡,加重KA诱导的神经病理过程。

     

    Abstract: Objective To study the association of leptin with the occurrence and development of temporal lobe epilepsy. Methods After injection of exogenous leptin, a normal dose of kainic acid (KA, 200 ng per mouse) were microinjected into the right hippocampus of C57BL/6J mice to induce temporal lobe epilepsy. Then, seizures were scored with the Racine scores,the hippocampal pathogenesis of mice on day 7 after the KA injection were observed, the expression level of Bax was measured by Western blot, the neuron loss of hippocampal Hilus was detected by Nissl staining, and the astrocyte activation and proliferation of hippocampal Hilus were tested by immunofluorescence method. Results Compared with KA-induced model, seizure scores increased by about 52%, the expression of Bax significantly increased by about 75%, the neuron loss significantly accelerated, and astrocyte was over activated in the KA-induced model combined with the exogenous leptin (10 mg/kg) pretreatment. Conclusion Leptin pretreatment aggravates the neuron apoptosis and pathogenesis induced by KA.

     

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