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| Content Provider | Springer Nature Link |
|---|---|
| Author | Zhu, Hong Can Gao, Xia Qun Xing, Ying Sun, Sheng Gang Li, Hong Ge Wang, Yun Fu |
| Copyright Year | 2004 |
| 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. |
| Starting Page | 299 |
| Ending Page | 305 |
| Page Count | 7 |
| File Format | |
| ISSN | 08958696 |
| Journal | Journal of Molecular Neuroscience |
| Volume Number | 24 |
| Issue Number | 2 |
| e-ISSN | 15591166 |
| Language | English |
| Publisher | Humana Press |
| Publisher Date | 2004-01-01 |
| Publisher Place | Totowa |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Neurosciences Neurology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Medicine Cellular and Molecular Neuroscience |
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