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Post-ischemic hypothermia-induced tissue protection and diminished apoptosis after neonatal cerebral hypoxia-ischemia

Artikel i vetenskaplig tidskrift
Författare Changlian Zhu
Xiaoyang Wang
X. Cheng
L. Qiu
F. Xu
G. Simbruner
Klas Blomgren
Publicerad i Brain Res
Volym 996
Nummer/häfte 1
Sidor 67-75
Publiceringsår 2004
Publicerad vid Institutionen för kvinnors och barns hälsa, Avdelningen för pediatrik
Institutionen för fysiologi och farmakologi, Avdelningen för fysiologi
Sidor 67-75
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Animals, Animals, Newborn, *Apoptosis, Body Temperature/physiology, Brain Infarction/etiology/pathology/*prevention & control, Caspases/metabolism, Cell Count/methods, Comparative Study, Cytochromes c/metabolism, DNA Fragmentation, Electron Transport Complex IV/metabolism, Female, *Hypothermia, Induced, Hypoxia-Ischemia, Brain/*complications, Immunoblotting/methods, Immunohistochemistry/methods, In Situ Nick-End Labeling/methods, Laterality, Male, Microtubule-Associated Proteins/metabolism, Random Allocation, Rats, Rats, Wistar, Research Support, Non-U.S. Gov't, Time Factors
Ämneskategorier Experimentell hjärnforskning, Neurobiologi

Sammanfattning

Hypothermia is possibly the single most effective method of neuroprotection developed to date. However, the mechanisms are not completely understood. The aim of this study was to investigate the effects of post-ischemic hypothermia on brain injury and apoptotic neuronal cell death as well as related biochemical changes after neonatal hypoxia-ischemia (HI). Seven-day-old rats were subjected to left common carotid artery ligation and hypoxia (7.8%) for 1 h. Systemic hypothermia was induced immediately after hypoxia-ischemia, and body temperature was maintained at 30 degrees C for 10 h. The normothermic group was kept at 36 degrees C. Brain infarct volumes and neuronal loss in the CA1 area of the hippocampus were significantly reduced at 72 h post-HI in the hypothermia group. Cytochrome c release and activation of caspase-3 and -2 at 24 h post-HI were significantly diminished by hypothermia. The numbers of cytochrome c- and TUNEL-positive cells in the cortex and dentate gyrus of the hippocampus were significantly reduced in the hypothermia group compared with the normothermia group at 72 h post-HI. These results indicate that hypothermia may, at least partially, act through inhibition of the intrinsic pathway of caspase activation in the neonatal brain, thereby preventing apoptotic cell death.

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