细胞凋亡的分子生化机制及其在Alzheimer's病发病中的作用

王润生;冯征;张均田

中国药学杂志 ›› 2001, Vol. 36 ›› Issue (05) : 289-292.

中国药学杂志 ›› 2001, Vol. 36 ›› Issue (05) : 289-292.
综述

细胞凋亡的分子生化机制及其在Alzheimer's病发病中的作用

  • 王润生;冯征;张均田
作者信息 +
文章历史 +

摘要

目的介绍凋亡及Alzhimer's 病(AD)的研究进展。方法选择近年来具有较高学术价值的国外文献,综述了在凋亡及AD方面的最新研究成果。结果与结论凋亡参与了许多体内的生理及病理过程。Bcl-2家族分子,细胞色素C,Caspase蛋白酶发挥主要的调节作用。另外凋亡过程参与了AD的病理过程。

关键词

细胞凋亡 / Bcl-2 / Bax / 细胞色素C / Caspases

引用本文

导出引用
王润生;冯征;张均田. 细胞凋亡的分子生化机制及其在Alzheimer's病发病中的作用[J]. 中国药学杂志, 2001, 36(05): 289-292

参考文献

[1]Perkins CL, Fang G, Kim CN, et al.The role of Apaf-1, caspase-9, and bid proteins in etoposide-or paclitaxel-induced mitochondrial events during apoptosis[J]. Cancer Res,2000,60(6):1645. [2]Zhivotovsky B,Orrenius S,Brustugun OT, et al.Injected cytochrome C induces apoptosis[J]. Nature,1998,391(6666):449. [3]Bossy-Wetzel E,Newmeyer DD,Green DR.Mitochondrial cytochrome C release in apoptosis occurs upstream of the DEVD-specific caspase activation and independently of mitochondrial transmembrane depolarization[J]. EMBO J,1998,17(1):37. [4]Li F,Srinivasan A,Wang Y,et al.Cell-specific induction of cytochrome C,Bcl-X(L)has activity independent of cytochrome C release[J]. J Biol Chem,1997,272(48):30299. [5]Reed JC.Cytochrome C:can’t live with it -can’t live without it.[J]Cell,1997,91(5):559. [6]Shimizu S,Narita M,Tsujimoto Y.Bcl-2 family proteins regulate the release of apoptogenic cytochrome C by the mitochondrial channel VDAC[J]. Nature,1999,399(6735):483. [7]Antonsson B, Montessuit S, Lauper S,et al.Bax oligomerization is equired for channel-forming activity in liposomes and to trigger cytochrome c elease from mitochondria[J]. Biochem J,2000,345(Pt 2):271. [8]Petit PX,Susin SA,Zamzami N,et al.Mitochondrial and programmed cell death:back to the future[J]. FEBS Lett,1996,396(1):7. [9]Vander Heiden MG,Chandel AS,Willianmson EK, et al.Bcl-X(L) regulates the membrane potential and volume homeostasis of mitochondria[J]. Cell,1997,91:627. [10]Yang J,Liu X,Bhalla K,et al.Prevention of apoptosis by Bcl-2:release of cytochrome C from mitochondria blocked[J]. Science,1997.275(5303):1129. [11]Rosse T,Oliver R,Monney L,et al.Bcl-2 prolongs cells suvival after Bax-induced release of cytochrome C[J]. Nature,1998,391(6666):496. [12]Okuno S,Shimizu S,Ito T,et al.Bcl-2 prevents caspase-independent cell death[J]. J Biol Chem,1998.273(51):34271. [13]Desagher S,Osen-Sand A,Nichols A,et al.Bid induced conformational change of bax is resposable for mitochopndrial cytochrome C release during apoptosis[J]. J Cell Biol,1999.144(5):891. [14]Miyashita T,Kitada S,Krajewski S,et al.Overexpression of the Bcl-2 protein increases the half-life of p21Bax[J]. J Biol Chem,1995.270(44):26049. [15]Enari M,Sakahira H,Nagata S.A caspase activited DNAse that degrades DNA during apoptosis[J]. Nature,1998.391(6662):43. [16]Cosulich SC,Savory PJ,Clarke PR.Bcl-2 regulates amplification of caspase activation by cytochrome C[J]. Curr Biol,1999.9(3):147. [17]Clem RJ,Cheng EH,Karp CL et al.Modulation of cell death by Bcl-X(L)through caspase interaction[J]. PNAS,1998,95(2):554. [18]Kirsch DG,Doseff A,Chau BN,et al. Caspase-3-dependent cleavage of Bcl-2 promotes release of cytochrome C[J]. J Biol Chem,1999,274(30):21155. [19]Tan J, Town T, Placzek A,et al.Bcl-X(L) inhibits apoptosis and necrosis produced by Alzheimer's beta-amyloid1-40 peptide in PC12 cells[J]. Neurosci Lett,1999,272(1):5. [20]Alberici A, Moratto D, Benussi L, et al.Presenilin 1 protein directly interacts with Bcl-2[J]. J Biol Chem,1999,274(43):30764. [21]Passer BJ, Pellegrini L, Vito P,et al.Interaction of Alzheimer's presenilin-1 and presenilin-2 with Bcl-X(L). A potential role in modulating the threshold of cell death[J]. J Biol Chem,1999,274(34):24007. [22]Tarkowski E, Blennow K, Wallin A,et al .Intracerebral production of tumor necrosis factor-alpha, a local neuroprotective agent, in Alzheimer disease and vascular dementia[J]. J Clin Immunol,1999 ,19(4):223. [23]Su JH, Deng G, Cotman CW.Bax protein expression is increased in Alzheimer's brain: correlations with DNA damage, Bcl-2 expression, and brain pathology[J]. J Neural Transm Suppl,1997,49:245. [24]Paradis E, Douillard H, Koutroumanis M,et al.Amyloid beta peptide of Alzheimer's disease downregulates Bcl-2 and upregulates bax expression in human neurons[J]. J Neurosci,1996,16(23):7533. [25]O'Barr S, Schultz J, Rogers J.Expression of the protooncogene bcl-2 in Alzheimer's disease brain[J]. Neurobiol Aging,1996,17(1):131. [26]Satou T, Cummings BJ, Cotman CW.Immunoreactivity for Bcl-2 protein within neurons in the Alzheimer's disease brain increases with disease severity[J]. Brain Res,1995,697(1-2):35. [ 27]Miranda S, Opazo C, Larrondo LF, et al. The role of oxidative stress in the toxicity induced by amyloid beta-peptide in Alzheimer's disease[J]. Prog Neurobiol,2000,62(6):633. [28]Pappolla MA, Chyan YJ, Poeggeler B, et al. An assessment of the antioxidant and the antiamyloidogenic properties of melatonin: implications for Alzheimer's disease[J]. J Neural Transm,2000;107(2):203. [29]Duan WZ, Zhang JT.Stimulation of central cholinergic neurons by (-)clausenamide in vitro[J]. Acta Pharmacol Sin,1998:19(4):332. [30]王润生,张均田.Baxα高表达PC12细胞系的建立及(-)黄皮酰胺抗细胞凋亡作用机制的研究[J].药学学报,2000,35(6):404.

基金

国家重点基础研究发展规划项目(973)资助课题(1998051109)

Accesses

Citation

Detail

段落导航
相关文章

/