The substantial increase in the number of elderly people in our societies represents a challenge for biology and medicine. The societies of the industrialized countries are subject to a progressive aging process that translates into an increase in the cardiovascular risk of the population. In the present work, the activity of catalase and superoxide dismutase was evaluated, as well as markers of oxidative stress (concentration of nitric oxide and total lipoperoxidation in its main components: malondialdehyde and 4-hydroxyalkene) in cardiomyocytes during the aging process in rats treated with resveratrol. Rats were divided into 4 groups according to the following categories: control (without treatment), negative control group (administered with physiological solution with 10% ethanol), positive control group (administered with vitamin E, 2 mg/kg/day), and group administered with resveratrol (10 mg/kg/day); these groups in turn were divided into 2, 4, 6, and 8 months of treatment. The analysis of nitric oxide showed a decreased level in the cardiac tissue in the groups treated with resveratrol; the same occurs when total lipoperoxidation is analyzed. The enzymatic activity studied (catalase and superoxide dismutase) did not present significant changes with respect to the controls. It is concluded that the cardioprotective effect of resveratrol is due to the antioxidant effect and other antiaging effects and not to the activation of the enzymes catalase and superoxide dismutase.
The increase in the elderly population has generated concern to meet health demands. The research efforts to elucidate the mechanisms of damage associated with aging have also been significantly increased, especially in order to avoid the reduction of the cognitive abilities in geriatric patients, resulting from the damage generated mainly at the level of the hippocampus during old age. At present, many studies describe resveratrol as an antiaging component. There are reports that it can activate the Sirt1 gene related to antiaging, emulating the effects obtained by caloric restriction in rodents. The aim of the study was to evaluate the effect of chronic administration of resveratrol (10 mg/kg) on cognitive performance in behavioral tests after 8 months of treatment and on the preservation of cerebral integrity in the cytoarchitecture of regions CA1 and CA2. Results showed that the cytoarchitecture of the CA1 and CA2 regions in the hippocampus retained their integrity over time in rats treated with resveratrol, and the behavioral test performed revealed that chronic resveratrol administration for 8 months showed improvements in cognitive performance. The results indicate that resveratrol may exhibit therapeutic potential for age-related conditions.
In the cerebral hypoxia-ischemia rat model, the prophylactic administration of zinc can cause either cytotoxicity or preconditioning effect, whereas the therapeutic administration of selenium decreases the ischemic damage. Herein, we aimed to explore whether supplementation of low doses of prophylactic zinc and therapeutic selenium could protect from a transient hypoxic-ischemic event. We administrated zinc (0.2 mg/kg of body weight; ip) daily for 14 days before a 10 min common carotid artery occlusion (CCAO). After CCAO, we administrated sodium selenite (6 μg/kg of body weight; ip) daily for 7 days. In the temporoparietal cerebral cortex, we determined nitrites by the Griess method and lipid peroxidation by the Gerard-Monnier assay. qPCR was used to measure mRNA of nitric oxide synthases, antioxidant enzymes, chemokines, and their receptors. We measured the enzymatic activity of SOD and GPx and protein levels of chemokines and their receptors by ELISA. We evaluated long-term memory using the Morris-Water maze test. Our results showed that prophylactic administration of zinc caused a preconditioning effect, decreasing nitrosative/oxidative stress and increasing GPx and SOD expression and activity, as well as eNOS expression. The therapeutic administration of selenium maintained this preconditioning effect up to the late phase of hypoxia-ischemia. Ccl2, Ccr2, Cxcl12, and Cxcr4 were upregulated, and long-term memory was improved. Pyknotic cells were decreased suggesting prevention of neuronal cell death. Our results show that the prophylactic zinc and therapeutic selenium administration induces effective neuroprotection in the early and late phases after CCAO.
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