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Component | Finding | (Year) Researchers |
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AIF | Translocation from mitochondria to nucleus produces DNA condensation. ↑ is correlated with ↑ infarct size (Rat model) | (2003) Zhu et al. [46] |
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AIF effect on DNA is nitric oxide independent (Rat Model) | (2004) Zhu et al. [47] |
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Hsp-70 ↓ translocation of AIF to the nucleus (Mouse model) | (2005) Matsumori et al. [48] |
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TAT-Bcl-xL ↓ AIF translocation to nucleus and caspase activation providing neuroprotection post HI (Rat model) | (2006) Yin et al. [49] |
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↑ nuclear translocation in males associated with ↑ injury Female mice show greater caspase 3 activity. (Mouse model) | (2006) Zhu et al. [50] |
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Hypothermia ↓ AIF translocation. (Rat model) | (2011) Askalan et al. [51] |
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Calpains | m-calpain but not μ-calpain cleaves caspase-3 (Rat model) | (2001) Blomgren et al. [52] |
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Calpain inhibition (using MDL28170) provides neuroprotection and ↓ necrosis (Rat model) | (2005) Kawamura et al. [53] |
Prolonged hypothermia ↓ calpain activation (Rat Model) | (2005) Ohmura et al. [54] |
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Polyphenols (pomegranate) provide neuroprotection and decrease calpain activation (Mouse model) | (2007) West et al. [55] |
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Inhibition produced by inhibition of JNK (using D-JNKI1) (Rat model) | (2009) Ginet et al. [56] |
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TAT-mGluR1 blocks the calpain cleavage site of mGluR1α and provide neuroprotection (Rat model) | (2009) Zhou et al. [57] |
Inhibition of JNK (using TAT-JBD) prevents calpain-mediated brain injury after HI (Rat model) | (2010) Nijboer et al. [41] |
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Calpain modulates the ↓ in Bcl-2 following HI (Rat model) | (2010) Zhu et al. [58] |
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Ethyl pyruvate is neuroprotective via inhibition of calpain activation and Ca2+ dysregulation. (Rat model) | (2010) Shen et al. [59] |
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Cathepsins | Propidium ioidide + cells in cortex and hippocampus were + for cathepsin B after HI suggesting necrosis (Rat model) | (2007) Carloni et al. [60] |
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Cathepsin D ↑ at 6 h and 24 h post-HI (Rat model) | (2009) Ginet et al. [56] |
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FADD | Expression is independent of gluthatione levels and hydrogen peroxide accumulation (Mouse model) | (2007) Payton et al. [61] |
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Inhibition of RIP-1 kinase activity restores the RIP-3/FADD interaction (Mouse model) | (2011) Northington et al. [7] |
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Fas-DR | ↑ in the thalamus following HI along with ↑ cleavage of caspase 8. (Rat model) | (2001) Northington et al. [62] |
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↑ after HI and genetic deletion provides neuroprotection to cortex (Mouse model) | (2004) Graham et al. [63] |
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Hsp-90 | — | No in vivo HI studies |
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Hsp-70 | Hsp-70 overexpression provide protection against apoptosis (Mouse model) | (2005) Matsumori et al. [48] |
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↑ FLIP levels, ↓ caspase-8 and 9 cleavage, and cytochrome C translocation to cytosol (Mouse model) | (2006) Matsumori et al. [64] |
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JNK | Activated after HI. Genetic deletion ↓ brain tissue loss. Activates c-JUN, ATF-2, Bim/PUMA (Mouse model) | (2007) Pirianov et al. [65] |
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Inhibition (using D-JNKI1), ↓ caspase-3 activation. (Rat model) | (2009) Ginet et al. [56] |
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Inhibition (using TAT-JBD) ↓ injury, improves outcomes, and preserves IAP (via inhibition of Smac/DIABLO). (Rat model) | (2010) Nijboer et al. [41] |
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p53 | ↑ in mitochondria→↑ cytochrome C and Smac/DIABLO translocation. ↓ p53 →↓ infarct (better outcomes). (Rat model) | (2011) Nijboer et al. [66] |
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PARP-1 | Activation after HI but ↓ NAD+ only in male mice and genetic deletion affords neuroprotection in males. (Mouse model) | (2004) Hagberg et al. [26] |
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Simvastatin ↓ PARP-1 activation and IL-1β expression and provides neuroprotection (Rat model) | (2006) Carloni et al. [67] |
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Immunoreactivity (IHC) peaks at 30 min and then again at 12 h post HI (Rat model) | (2005) Martin et al. [68] |
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RIP1/RIP3 | ↓ complex (necrosome) formation by necrostatin after HI affords neuroprotection, ↓ oxidation and FLIP (Mouse model) | (2011) Northington, et al. [7] |
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TNFR | NF-κB inhibition ↓ brain damage and switches the HI-induced TNF-R profile from ↑ TNF-R1 to ↑ TNF-R2. (Rat model) | (2009) Nijboer et al. [69] |
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TRADD | — | No in vivo HI studies |
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