Acta Academiae Medicinae Sinica

Acta Academiae Medicinae Sinica

Acta Academiae Medicinae Sinica ›› 2011, Vol. 33 ›› Issue (6): 659-662.doi: 10.3881/j.issn.1000-503X.2011.06.015

• Original Articles • Previous Articles     Next Articles

Role of β-catenin in the Pathogenesis of Mesial Temporal Lobe Epilepsy

XING Xiao-liang1, SHA Long-ze1, ZHANG Dan2, SHEN Yan1, WU Li-wen2, XU Qi1   

  1. 1National Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences,CAMS and PUMC, Beijing 100005, China; 2 Department of Neurology,PUMC Hospital, CAMS and PUMC, Beijing 100730, China
  • Received:2011-10-25 Revised:2012-01-04 Online:2011-12-20 Published:2011-12-20
  • Contact: XU Qi
  • Supported by:

    Supported by the National Natural Sciences Foundation of China (30971001, 31021091) , the Beijing Natural Science Foundation (7102109) , and the Fok Ying Tong Education Foundation (121024)

Abstract: Objective To explore the role of β-catenin in the pathogenesis of mesial temporal lobe epilepsy. Methods Kainic acid-induced rat models of medial temporal lobe epilepsy was established. The expression of β-catenin in the normal mice and the model mice were detected using Western blot analysis. The expression of β-catenin at human hippocampus was detected using immunohistochemical analysis and immunofluorescence and compared between patients with non-hippocampal sclerosis temporal lobe epilepsy and those with hippocampal sclerosis epilepsy. Results The pathologies of model mice were similar with those in mice with hippcampal sclerosis temporal lobe epilepsy, demonstrating that the mice model was successfully established. Western blot analysis showed no significant difference of β-catenin expression between normal mice and model mice. As shown by immunohistochemical analysis and immunofluorescence, β-catenin expression in human hippocampus was also not significantly different between patients with temporal lobe epilepsy without hippocampal sclerosis and those with hippcampal sclerosis. Conclusion β-catenin may not be involved in the development of hippocampal sclerosis of mesial temporal lobe epilepsy.

Key words: mesial temporal lobe epilepsy, hippocampal sclerosis, β-catenin, kainic acid, C57BL/6 mice

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