1[1]Li Y,Chopp M, Jiang N,et al. Temporal profile of in situ DNA fragmentation after transient middle cerebral artery occlusion in the rat. J Cere Blood Flow Metab,1995,15:389~397.
2[2]Charriaut-marlangue C, Margaill I, Represa A,et al. Apoptosis and neurosis after reversible focal ischemia: an in situ DNA fragmentation analysis. J Cere Blood Flow Metab, 1996,16:186~194.
3[3]Chen J, Nagayama T, Jin K,et al. Induction of caspase-3 like protease may mediate delayed death in the hippocampus after transient cerebral ischemia. J Neurosci,1998,18:4 914~4 928.
4[4]Namura S, Zhu J, Fink K,et al. Activation and cleavage of caspase-3 in apoptosis induced by experimental cerebral ischemia. J Neurosic,1998,18:3 659~3 668.
5[5]Frykholn P, Andersson JLR, Valtysson J, et al. A metabolic threshold of irreversible ischemia demonstrated by PET in a middle cerebral artery occlusion reperfusion model. Acta Neurol Scand,2000,102(1):18~26.
6[6]Hunter DR,Haworth RA.The Ca2+-induced membrane transition in mitochondria.Ⅱ. Nature of the Ca2+ trigger site. Arth Biochem Biophys,1979,195(2):453~459.
7[7]Fournier N, Ducet G, Crevat A. Action of cyclosporin on mitochondrial calcium flures. J Bioenerg Biomember,1987,19:297~303.
8[8]Petit P.X, Leceur H, Zorn E, et al. Alterations in mitochondrial structure and function are early events of dexamethasone-induced thymocyte apoptosis. J Cell Biol,1995,130:157~167.
9[9]Li P.A, Uchino H, Elmer E, et al. Amelioration by cyclosporin c of brain damage following 5 and 10 min of ischemia in rat subjected to preischemic hyperglycemia. Brain research,1997,753:133~140.
10[10]Matsumoto S, Friberg H, Ferrand M, et al. Blockade of the mitochondrial permeability transition pore diminishes infarct size in the rat after transient cerebral artery occlusions. J Cere Blood Metab,1999,19:736~741.