Alpha-tocopherol in the brain tissue preservation of stroke-prone spontaneously hypertensive rats.
Oxidative stress has an important role in neuronal damage during cerebral ischemia and can lead to cognitive and behavioral impairment. Alpha-tocopherol, a powerful antioxidant, may be able to preserve neuronal tissue and circumvent neurological deficits. Thus, this study aimed to investigate the influence of alpha-tocopherol in the preservation of brain tissue and the maintenance of memory formation in stroke-prone spontaneously hypertensive rats (SHRSP). To achieve this aim, twenty-four 15-week-old male SHRSP rats were separated into the following four groups (n = 6 each) that received different treatments over a 4-week period: the alpha-tocopherol group, the control group, the L-NAME group, and the L-NAME + alpha-tocopherol group. We evaluated the physiological parameters (body weight, diuresis, and food and water intake), an oxidative stress marker (malondialdehyde levels), and neurological responses (the Morris Water Maze and Novel Objects Recognition tests). Afterwards, the brains were removed for histopathological analysis and quantification of the number of cells in the hippocampus. Statistically, the alpha-tocopherol group demonstrated better results when compared to all groups. The data indicated a reduction in oxidative stress and the preservation of neurological responses in groups treated with alpha-tocopherol. In contrast, the L-NAME group exhibited increased malondialdehyde levels, impairment of neurological responses, and several hippocampus tissue injuries. The others groups exhibited nerve tissue changes that were restricted to the glial nodes. No significant alterations were observed in the physiologic parameters. Based on these findings, we suggest that alpha-tocopherol can prevent stroke, preserve the structure of the hippocampus, and maintain both memory and cognition functions.
Laboratory of Nutritional Investigation and Degenerative-Chronic Diseases, Federal University of Rio de Janeiro State (Doctoral Program in Neurology - UNIRIO), 290 Xavier Sigaud Street, Urca, Rio de Janeiro, Rio de Janeiro, 22290-240, Brazil, leomurad@ig.com.br.
Leonardo Borges
LB
Murad
Marcela Rodrigues Moreira
MR
Guimarães
Aline
A
Paganelli
Carlos Alberto Basílio
CA
de Oliveira
Lucia Marques
LM
Vianna
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology* / Q000627:therapeutic use; D002545:Brain Ischemia / Q000188:drug therapy* / Q000378:metabolism / Q000523:psychology; D002452:Cell Count; D004353:Drug Evaluation, Preclinical; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018782:Maze Learning; D008570:Memory, Short-Term / Q000187:drug effects; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009474:Neurons / Q000187:drug effects; D018696:Neuroprotective Agents / Q000494:pharmacology* / Q000627:therapeutic use; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D018384:Oxidative Stress; D051381:Rats; D011918:Rats, Inbred SHR; D021641:Recognition, Psychology / Q000187:drug effects; D024502:alpha-Tocopherol / Q000494:pharmacology* / Q000627:therapeutic use
D000975:Antioxidants; D018696:Neuroprotective Agents; D008315:Malondialdehyde; D019001:Nitric Oxide Synthase; D024502:alpha-Tocopherol; D019331:NG-Nitroarginine Methyl Ester