Oxidative stress after traumatic brain injury may contribute to many of the pathophysiologic changes. Resveratrol, naturally present at high concentration in grape skin, seeds, and red wine, has significant antioxidant properties in a variety of in vitro and in vivo models. In this study, we investigate the effect of resveratrol on oxidative stress after traumatic brain injury in rat model.A total of 54 adult Wistar albino male rats weighing 250-300 g were used. The rats were allocated into three groups. The first group was control (sham-operated) group in which only a craniotomy was performed, the others were trauma and resveratrol groups. A 100 mg/kg single dose of resveratrol, freshly prepared by dissolving in 50% ethanol and diluted in physiological saline (2%), for resveratrol group, and 1 ml ethanol (2%) for trauma group, was administered intraperitoneally immediately after trauma. Weight-drop method was used for achieving head trauma. Then, all groups were separated into three subgroups for biochemical analysis, brain water content and histopathological assessment following trauma. Twenty-four hours after trauma brain water content and malondialdehyde (MDA), glutathione (GSH), nitric oxide (NO), xanthine oxidase (XO) levels of traumatic hemisphere were evaluated. Quantitative histopathological analysis was performed on 14th day postinjury. Trauma caused a significant increase in MDA, XO, NO levels and decrease in GSH level as compared to control group. Resveratrol administration significantly reduced MDA, XO and NO levels, increased GSH level, and also attenuated tissue lesion area. Our results indicate that treatment with resveratrol immediately after traumatic brain injury reduce oxidative stress and lesion volume. Future studies involving different doses and the dose-response relationship could promise better results.

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Aim: To investigate the neuroprotective effect of resveratrol in an experimental spinal cord injury (SCI) model in rats. Methods: Male Wistar albino rats weighing 200-250 g were randomized into six groups. Weight-drop trauma was performed for SCI. Group 1 underwent laminectomy alone. Group 2 underwent laminectomy followed by SCI. Groups 3, 4, 5, and 6 underwent laminectomy followed by SCI and received resveratrol (100 mg/kg), methylprednisolone (MP) (30 mg/kg), resveratrol (100 mg/kg) plus MP (30 mg/kg), and ethanol (2%), respectively. The rats were divided into two subgroups for biochemical analysis (killed at 24 h after surgery) and for neurobehavioral and histopathological evaluation (killed at 6 weeks after surgery). Posttraumatic neurological recovery after surgery was recorded weekly. Results: Groups 3 and 5 revealed significantly lower malondialdehyde, nitric oxide, xanthine oxidase, and higher glutathione levels than group 4 (P<0.05). Neurological recovery rates were significantly better in groups 3 and 5 than group 4 (P<0.05). When spinal trauma size ratios were compared, there was no significant difference between treatment groups. Conclusion: Resveratrol treatment revealed better biochemical recovery in the acute stage of trauma than MP treatment. Although resveratrol and combined treatment revealed better neurobehavioral recovery than MP treatment; resveratrol, MP, and combined treatment modalities improved histopathological recovery at the same level in the final stage of the experiment. Future studies involving different doses of resveratrol and different doses combinations with MP could promise better results as each drug has a different anti-oxidative mechanism of action.

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Breast cancer (BCa) was induced in vivo in female rats with 7,12-dimethylbenz(a)anthracene (DMBA). Two main questions were addressed. Firstly, would the carcinogenesis be accompanied by oxidative stress as signalled by superoxide dismutase, glutathione peroxidase, malondialdehyde and total nitrate? Secondly, would treating the rats additionally with a blocker of voltage-gated sodium channel (VGSC) activity, shown previously to promote BCa progression, affect the oxidative responses? The DMBA-induced increases in the antioxidant systems were completely blocked by the VGSC inhibitor RS100642, which also significantly prolonged the lifespan. We conclude that VGSC inhibition in vivo can significantly protect against oxidative stress and improve survival from tumour burden.