Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing Key Laboratory of Neurology, 1st Youyi Road, Chongqing 400016, China.
Peptides. 2011 Sep;32(9):1793-9. doi: 10.1016/j.peptides.2011.08.006. Epub 2011 Aug 16.
Prolonged epileptic seizures or SE can cause neuronal cell death. However, the exact role of neuroprotectant against brain injury during epileptic seizure needs to be further elucidated. The aim of this study was to investigate the expression of the apelin, a novel neuroprotective peptide, in brain tissues of the patients with temporal lobe epilepsy (TLE) and experimental rats using immunohistochemistry, immunofluorescence and Western blotting analysis and to discuss the possible role of apelin in TLE. Thirty temporal neocortical tissue samples from the patients with drug-refractory TLE underwent surgical therapy and nine histologically normal temporal lobes tissues as controls were used in our study. Fifty-six Sprague-Dawley rats were randomly divided into seven groups, including one control group and six groups with epilepsy induced by lithium-pilocarpine. Hippocampus and adjacent cortex were taken from the controls and epileptic rats at 1, 3, 7, 14, 30, and 60 days after onset of seizures. Apelin was mainly expressed in the neurons of TLE patients and controls, and was significantly increased in TLE patients compared with the controls. Apelin was also expressed in the neurons of experimental and control rats, it was gradually increased in the experimental rat post-seizure and reached a stable high level in chronic epileptic phase. Our results demonstrated that the increased expression of apelin in the brain may be involved in human TLE.
癫痫持续发作或 SE 可导致神经元细胞死亡。然而,神经保护剂在癫痫发作期间对脑损伤的确切作用仍需进一步阐明。本研究旨在通过免疫组织化学、免疫荧光和 Western blot 分析,研究阿片肽(一种新型神经保护肽)在颞叶癫痫(TLE)患者和实验大鼠脑组织中的表达,并探讨阿片肽在 TLE 中的可能作用。我们的研究使用了 30 例药物难治性 TLE 患者的颞叶皮质组织样本(来自接受手术治疗的患者)和 9 例组织学正常的颞叶组织作为对照。56 只 Sprague-Dawley 大鼠随机分为 7 组,包括 1 组对照组和 6 组匹罗卡品锂诱导癫痫组。在癫痫发作后 1、3、7、14、30 和 60 天,从对照组和癫痫大鼠中取出海马和邻近皮质用于检测。阿片肽主要在 TLE 患者和对照组的神经元中表达,并且在 TLE 患者中明显高于对照组。阿片肽也在实验大鼠和对照组大鼠的神经元中表达,在癫痫发作后逐渐增加,并在慢性癫痫期达到稳定的高水平。我们的研究结果表明,大脑中阿片肽表达的增加可能与人类 TLE 有关。