共 18 条
[1]
Post - ischemichypothermia blocks caspase-3 activation in the newbom rat brainafter hypoxia-ischemia. Fukuda H,Tomimatsu T,Watanabe N,et al. Brain Research . 2001
[2]
Mitochondria and apoptosis. Green DR,Reed JC. Science . 1998
[3]
Caspase inhibitor affordsneuroprotection with delayed administration in a rat model ofneonatal hypoxic-ischemic brain injury. Cheng Y,Deshmukh M,D’Costa A,et al. The Journal of Clinical Investigation . 1998
[4]
Impairment ofmitochondrial respiration after cerebral hypoxia-ischemia inimmature rats: relationship to activation of caspase-3 and neuronalinjury. Puka-Sundvall M,Wallin C,Gilland E,et al. Brain Research Developmental Brain Research . 2000
[5]
Effects of hypothermiaon neonatal hypoxic-ischemicbrain injury in the rat:phosphory-lation of Akt, activation of caspase-3-like protease. Tomimatsu T,Fukuda H,Endo M,et al. Neuroscience Letters . 2001
[6]
Mild hypothermia reducesapoptosis of mouse neurons in vitro early in the cascade. Xu L,Yenari MA,Steinberg GK,et al. Journal of Cerebral Blood Flow and Metabolism . 2002
[7]
BDNF protects the neonatal brain from hypoxic-ischemic injury in vivo via the ERK pathway. Han BH,Holtzman DM. The Journal of Neuroscience . 2000
[8]
Caspase-3 activation afterneonatal rat cerebral hypoxia-ischemia. Wang X,Karlsson JO,Zhu C,et al. Biology of the Neonate . 2001
[9]
Involvement of caspase-3 incell death after hypoxia-ischemia declines during brain maturation. Hu BR,Liu CL,Ouyang Y,et al. Journal of Cerebral Blood Flow and Metabolism . 2000
[10]
The changing landscape of ischemic brain injury mechanisms. Lee JM,Zipfel GJ,Choi DW. Nature .