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  • Title: Inhibition of caspase-3 activation and apoptosis is involved in 3-nitropropionic acid-induced ischemic tolerance to transient focal cerebral ischemia in rats.
    Author: Zhu HC, Gao XQ, Xing Y, Sun SG, Li HG, Wang YF.
    Journal: J Mol Neurosci; 2004; 24(2):299-305. PubMed ID: 15456943.
    Abstract:
    Our aim was to investigate the involvement of caspase-3 activation and apoptotic cell death in mitochondrial toxin 3-nitropropionic acid (3-NPA)-induced ischemic tolerance to transient focal cerebral ischemia in rats. Rats were administrated either vehicle control or 3-NPA ip doses of 20 mg/kg. Three days later, rats were exposed to 2 h of middle cerebral artery occlusion, followed by 24 h of reperfusion. Infarct volumes were assessed by 2,3,5-triphenyltetrazolium chloride (TTC) staining 24 h after reperfusion. We measured neural cell apoptosis in the cerebral ischemic penumbra by terminal deoxynucleotidyl transferase-mediated dUTP-biotin in situ nick end labeling (TUNEL) and flow cytometry (FCM). Cleavage of the fluorogenic substrate zDEVD-afc was used to assay caspase-3 activity. Compared with the vehicle-injected group, pretreatment with 3-NPA reduced the infarct volume by 22.3% and decreased the number of TUNEL-positive neural cells and apoptotic percentages by 47% (p <0.05) and 43.9% (p <0.01), respectively. In terms of caspase-3 activity in ischemic penumbral tissues, the 3-NPA-pretreated group showed 13.9% (p <0.05) less caspase-3 activity than the control group. The development of 3-NPA-induced ischemic tolerance in brain may be related to decreases in caspase-3 activation, which leads to decreased neural cell apoptosis.
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