Experimental treatment for focal hyperglycemic ischemic brain injury in the rat

• Hyperglycemia aggravates ischemic brain injury, possibly due to the activation of signaling pathways involving reactive oxygen species, Src and mitogen-activated protein kinases. The aim of this study was to investigate the effects of the spin trap agent alpha-phenyl-N-tert-butyl nitrone (PBN), the Src family kinase inhibitor PP2 and the MEK1-inhibitor U0126 on focal hyperglycemic ischemic brain injury. Temporary middle cerebral artery occlusion (90 min) was induced in four groups of rats (PBN, PP2, and U0126 vs. control). Neurological testing and tetrazolium red staining were performed after 1 day. PBN decreased the infarct volume by 70% compared with the control (P<0.05) and a tendency towards reduced infarcts was seen in the PP2 or U0126 groups. Furthermore, neurological testing was consistent with the volumetric analysis. In conclusion, PBN appears to be a potential neuroprotective agent in hyperglycemic, focal ischemic brain injury, while the efficacy of PP2 and U0126 could not be confirmed by the present data.

Nyckelord

Animals

Blood Glucose/physiology

Body Temperature/physiology

Brain Ischemia/pathology/*prevention & control

Butadienes/therapeutic use

Carbon Dioxide/blood

Comparative Study

Enzyme Inhibitors/therapeutic use

Hyperglycemia/*complications/pathology

Male

Neurologic Examination/methods

Neuroprotective Agents/*therapeutic use

Nitriles/therapeutic use

Nitrogen Oxides/*therapeutic use

Oxygen/blood

Pyrimidines/therapeutic use

Rats

Rats; Sprague-Dawley

Research Support; Non-U.S. Gov't

Tetrazolium Salts/diagnostic use

Time Factors

Publikations- och innehållstyp

ref (ämneskategori)

art (ämneskategori)