钾通道在Aβ_(1-40)诱导的NSC凋亡中的作用
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- 论文作者：王国辉 ; 陆晓红 ; 阴育红
- 年：2017
- 作者机构：佳木斯大学附属第一医院;佳木斯市中心医院;
- 会议召开时间：2017-05-26
- 会议录名称：2017年《中国组织化学与细胞化学杂志》临床研讨会论文集
- 语种：中文
- 分类号：R749.16
- 学会代码：ZHXB
- 会议名称：2017年《中国组织化学与细胞化学杂志》临床研讨会
- 会议地点：中国湖北武汉
- 主办单位：《中国组织化学与细胞化学杂志》社有限公司
- 学会名称：《中国组织化学与细胞化学杂志》社有限公司
- 页数：1
- 文件大小：138k
- 原文格式：O
- 会议级别：全国
摘要
<正>凋亡,即程序性细胞死亡,在正常情况下可促进组织细胞发育和保持动态平衡,但是在某些化学、物理、环境或遗传学方面的损伤因素作用下可介导病理性细胞死亡~([1]),这种病理性调控在某些疾病状态下尤为突出,如癌症的病因学,AIDS,自身免疫性疾病和神经退行性病变如阿尔茨海默病(AD)和帕金森氏病(PD)等~([2])。最初凋亡是通过形态学特征定义的,包括胞体缩小,核浓缩,染色质边缘化,DNA片段化及凋亡小体的形
引文
[1]Raff,M.C.,Barres,B.A.,Burne,J.F.,Coles,H.S.,Ishizaki,Y.,Jacobson,M.D.,1993.Programmed cell death and the control of cell survival;lessons from the nervous system.Science 262,695-700.
[2]Singh N,Anand S.Apoptosis in health and disease.Indian J Physiol Pharmacol.1995 Apr;39(2):91-94.
[3]Kerr,J.F.,Wyllie,A.H.,Currie,A.R.,1972.Apoptosis;a basic biological phenomenon with wide-ranging implications in tissue kinetics.Br.J.Cancer 26,239-257.
[4]Etcheberrigaray R,Ito E,Oka K,Tofel-Grehl B,Gibson GE and Alkon DL(1993)Potassium channel dysfunction in fibroblasts identifies patients with Alzheimer disease.Proc Nad Acad Sci USA 90:8209-8213.
[5]Jin HW,Zhang W,Wang XL.Effects of chronic exposure to beta-amyloid-peptide25-35 on the mRNA expressions of voltage-gated outward potassium channel subunits in cultured rat hippocampal neurons.Acta Pharm.Sin.2002 Aug;37(8):598-602.
[6]Takuma H,Tomiyama T,Kuida K,Mori H.Amyloid beta peptide-induced cerebral neuronal loss is mediated by caspase-3 in vivo.J Neuropathol Exp Neurol.2004 Mar;63(3):255-61.21.
[7]Su JH,Anderson AJ,Cribbs DH,Tu C,Tong L,Kesslack P,Cotman CW.Fas and Fas ligand are associated with neuritic degeneration in the AD brain and participate in beta-amyloid-induced neuronal death.Neurobiol Dis.2003 Apr;12(3):182-93.
[8]Colom,L.V.,Diaz,M.E.,Beers,D.R,Neely,A.,Xie,W.J.,Appel,S.H.,1998.Role of potassium channels in amyloid-induced cell death.J.Neurochem.70,1925-1934.
[2]Singh N,Anand S.Apoptosis in health and disease.Indian J Physiol Pharmacol.1995 Apr;39(2):91-94.
[3]Kerr,J.F.,Wyllie,A.H.,Currie,A.R.,1972.Apoptosis;a basic biological phenomenon with wide-ranging implications in tissue kinetics.Br.J.Cancer 26,239-257.
[4]Etcheberrigaray R,Ito E,Oka K,Tofel-Grehl B,Gibson GE and Alkon DL(1993)Potassium channel dysfunction in fibroblasts identifies patients with Alzheimer disease.Proc Nad Acad Sci USA 90:8209-8213.
[5]Jin HW,Zhang W,Wang XL.Effects of chronic exposure to beta-amyloid-peptide25-35 on the mRNA expressions of voltage-gated outward potassium channel subunits in cultured rat hippocampal neurons.Acta Pharm.Sin.2002 Aug;37(8):598-602.
[6]Takuma H,Tomiyama T,Kuida K,Mori H.Amyloid beta peptide-induced cerebral neuronal loss is mediated by caspase-3 in vivo.J Neuropathol Exp Neurol.2004 Mar;63(3):255-61.21.
[7]Su JH,Anderson AJ,Cribbs DH,Tu C,Tong L,Kesslack P,Cotman CW.Fas and Fas ligand are associated with neuritic degeneration in the AD brain and participate in beta-amyloid-induced neuronal death.Neurobiol Dis.2003 Apr;12(3):182-93.
[8]Colom,L.V.,Diaz,M.E.,Beers,D.R,Neely,A.,Xie,W.J.,Appel,S.H.,1998.Role of potassium channels in amyloid-induced cell death.J.Neurochem.70,1925-1934.