Neural Regeneration Research ›› 2012, Vol. 7 ›› Issue (14): 1095-1100.

Previous Articles     Next Articles

Overexpression of estrogen receptor beta alleviates the toxic effects of beta-amyloid protein on PC12 cells via non-hormonal ligands

Hui Wang1, Lihui Si2, Xiaoxi Li3, Weiguo Deng4, Haimiao Yang5, Yuyan Yang6, Yan Fu1   

  1. 1 Department of Gynaecology and Obstetrics, First Hospital of Jilin University, Changchun 130021, Jilin Province, China
    2 Department of Gynaecology and Obstetrics, Second Hospital of Jilin University, Changchun 130044, Jilin Province, China
    3 Department of Gynaecology, Affiliated Hospital of Changchun University of Traditional Chinese Medicine, Changchun 130021, Jilin Province, China
    4 Department of Children’s Heatlh, School of Public Health, Jilin Univeristy, Changchun 130021, China
    5 Department of Scientific Research, Affiliated Hospital of Changchun University of Traditional Chinese Medicine, Changchun 130021, China
    6 Department of Gynaecology and Obstetrics, Minzu Hospital of Yitong County, Yitong 130700, Jilin Province, China
  • Received:2012-03-31 Revised:2012-04-23 Online:2012-05-15 Published:2012-05-15
  • Contact: Yan Fu, M.D., Chief physician, Department of Gynaecology and Obstetrics, First Hospital of Jilin University, Changchun 130021, Jilin Province, China
  • About author:Hui Wang☆, M, D., Attending physician, Department of Gynaecology and Obstetrics, First Hospital of Jilin University, Changchun 130021, Jilin Province, China

PDF

950

Abstract:

After binding to the estrogen receptor, estrogen can alleviate the toxic effects of beta-amyloid protein, and thereby exert a therapeutic effect on Alzheimer’s disease patients. Estrogen can increase the incidence of breast carcinoma and endometrial cancer in post-menopausal women, so it is not suitable for clinical treatment of Alzheimer’s disease. There is recent evidence that the estrogen receptor can exert its neuroprotective effects without estrogen dependence. Real-time quantitative PCR and flow cytometry results showed that, compared with non-transfected PC12 cells, adenovirus-mediated estrogen receptor β gene-transfected PC12 cells exhibited lower expression of tumor necrosis factor α and interleukin 1β under stimulation with beta-amyloid protein and stronger protection from apoptosis. The Akt-specific inhibitor Abi-2 decreased the anti-inflammatory and anti-apoptotic effects of estrogen receptor β gene-transfection. These findings suggest that overexpression of estrogen receptor β can alleviate the toxic effect of beta-amyloid protein on PC12 cells, without estrogen dependence. The Akt pathway is one of the potential means for the anti-inflammatory and anti-apoptotic effects of the estrogen receptor.

Key words: estrogen, estrogen receptor β, Alzheimer's disease, beta-amyloid protein, adenovirus, neural re-generation