n-acetylcarnosine and Subarachnoid-Hemorrhage

The neuroprotective effect of N-acetylcysteine (NAC), a sulfhydryl-containing antioxidant, on experimentally induced subarachnoid hemorrhage (SAH) in rats was assessed. NAC was administered to rats after the induction of SAH. Neurological deficits and brain edema were investigated. The activity of antioxidant defense enzymes, copper/zinc superoxide dismutase (CuZn-SOD) and glutathione peroxidase (GSH-Px), were measured in the brain cortex by spectrophotometer. The content of the lipid peroxidation product malondialdehyde (MDA) was also analyzed. We found that NAC markedly reversed the SAH-induced neurological deficit and brain edema. We further investigated the mechanism involved in the neuroprotective effects of NAC on rat brain tissue and found that NAC significantly increased CuZn-SOD and GSH-Px activity and decreased MDA content in the SAH brain. NAC has the potential to be a novel therapeutic strategy for the treatment of SAH, and its neuroprotective effect may be partly mediated via enhancing the activity of endogenous antioxidant enzymes and inhibiting free radical generation.

Topics: Analysis of Variance; Animals; Brain Edema; Carnosine; Cerebral Cortex; Disease Models, Animal; Gene Expression Regulation; Glutathione Peroxidase; Lipid Peroxidation; Male; Malondialdehyde; Nervous System Diseases; Neuroprotective Agents; Oxidative Stress; Rats; Rats, Sprague-Dawley; Subarachnoid Hemorrhage; Superoxide Dismutase