Strength training or green tea prevent memory deficits in a ß-amyloid peptide-mediated Alzheimer's disease model.

Antioxidant supplementation and physical exercise have been discussed as strategies to minimize neurodegeneration in Alzheimer's disease (AD). We investigated the neuroprotective effects of strength exercise (StrEx) and green tea (GT) supplementation, combined or not, on memory impairments induced by ß-amyloid characterizing an AD-like condition in rats. Wistar rats were submitted to 8 weeks of StrEx, GT supplementation, or StrEx and GT combined. AD-like condition was induced by injection of Aß (25-35) in the hippocampus. We evaluate object recognition (OR) and social recognition (SR) memory, and removed the rats' hippocampus for biochemical analysis. StrEx improved OR and SR. StrEx combined with GT improved OR and did not improve SR. GT reduced antioxidant capacity and improved acetylcholinesterase activity. Both strength exercise and green tea are neuroprotective against impairments resultant of ß-amyloid, but benefits do not add up when the two interventions are associated.

Green Tea and Red Tea from Camellia sinensis Partially Prevented the Motor Deficits and Striatal Oxidative Damage Induced by Hemorrhagic Stroke in Rats.

Green tea from Camellia sinensis plays a well-established neuroprotective role in several neurodegenerative diseases, including intracerebral hemorrhage (ICH). However, the other teas of the same plant do not have their properties well understood; but they can be as effective as green tea as an alternative therapy. In this study, we investigated the effects of supplementation with green tea and red tea from Camellia sinensis on motor deficits and striatum oxidative damage in rats submitted to hemorrhagic stroke (ICH). Male Wistar rats were supplemented with green tea, red tea, or vehicle for 10 days prior to ICH induction. After injury, the rats were submitted to motor tests (open field for locomotion, rotarod for balance, and neurological deficit scale (NDS)) 1, 3, and 7 days after ICH induction, while the tea supplementation was maintained. Subsequently, the rats were euthanized to striatal tissue dissection for biochemical analyzes (lipid peroxidation, reactive oxygen species, glutathione levels, and total antioxidant capacity). ICH caused locomotor and balance deficits, as well as increased the neurological deficit (NDS). Only red tea prevented locomotor deficits after injury. Green tea and red tea prevented balance deficits on the seventh day after ICH. On NDS evaluation, green tea presented a better neuroprotection than red tea (until day 3 after ICH injury). In addition, ICH increased reactive oxygen species and lipid peroxidation levels, without altering antioxidant markers. Green and red teas were effective in decreasing the lipid peroxidation levels. Therefore, green and red teas partially prevented the motor deficits and striatal oxidative damage induced by ICH. Based on our results, we can consider that the two teas seem to be equally effective to prevent motor deficits and striatal oxidative damage induced by hemorrhagic stroke in rats.

Effect of green tea extract supplementation on exercise-induced delayed onset muscle soreness and muscular damage.

Previous studies addressed the antioxidant and anti-inflammatory role of compounds from green tea in different human tissues. Positive antioxidant and anti-inflammatory effects were described for brain tissues. Whether similar effects are observed in the skeletal muscle, green tea supplementation could be a strategy to reduce delayed onset muscle soreness resultant of exercise. Here we determine the effect of green tea extract supplementation on exercise-induced muscle soreness, muscle damage and oxidative stress. We performed a randomized triple blind placebo control study. Twenty non-trained men performed sessions of exercise to induce delayed onset muscle soreness in the triceps sural muscle group before and after 15 days of supplementation (500 mg/day) with green tea extract (n = 10) or a placebo (n = 10). Muscle soreness was evaluated using a visual scale. Blood samples were taken at different moments to determine serum blood markers of muscle damage, oxidative stress and antioxidant status. We found that exercise induced delayed onset muscle soreness. Supplementation reduced muscle damage but muscle soreness did not change. Plasma oxidative damage marker and antioxidant status did not show an effect of supplementation. As a conclusion, green tea extract supplementation did not reduce the sensation of delayed onset muscle soreness but reduces the marker of muscle damage after exercise. It suggests the green tea extract supplementation has positive effects on muscle recovery after strenuous exercise.

Green tea supplementation produces better neuroprotective effects than red and black tea in Alzheimer-like rat model.

Green tea from Camellia sinensis plays a neuroprotective role in different neurodegenerative conditions, such as memory deficits in Alzheimer disease (AD). However, whether other teas from Camellia sinensis present similar neuroprotective effect still is not clear. Here we investigate effects of green, red and black tea supplementation on memory and hippocampus oxidative status in a rat model of Alzheimer-like disease (AD-like). METHOD: Wistar male rats were supplemented with green, red or black tea during 8weeks before Aß intra-hippocampal injection (2µL of Aß-25-35, CA1 region). AD and sham rats were submitted to memory tests. After euthanasia, oxidative status in the bilateral hippocampus was quantified. Green and red teas avoid memory deficits in AD rats, but only green tea also avoids oxidative stress and damage in the hippocampus. Green tea was more effective for neuroprotection than red and black teas from the Camellia sinensis in the AD rat model.

Supplementation with different teas from Camellia sinensis prevents memory deficits and hippocampus oxidative stress in ischemia-reperfusion.

Memory and cognition impairments resultant of ischemic stroke could be minimized or avoided by antioxidant supplementation. In this regard, the neuroprotective potential of Green tea from Camellia sinensis has been investigated. However, there is a lack of information regarding the neuroprotective potential of others teas processed from the Camellia sinensis. Here we investigate the neuroprotective role of green, red, white and black tea on memory deficits and brain oxidative stress in a model of ischemic stroke in rats. Our findings show that green and red teas prevent deficits in object and social recognition memories, but only green tea protects against deficits in spatial memory and avoids hippocampal oxidative status and intense necrosis and others alterations in the brain tissue. In summary, green tea shows better neuroprotection in ischemic stroke than the others teas from Camellia sinensis.

Short-term green tea supplementation prevents recognition memory deficits and ameliorates hippocampal oxidative stress induced by different stroke models in rats.

This study investigated the effect of green tea (GT) on short and long term declarative memory and oxidative damage induced by transient ischemia-reperfusion (IR) and intracerebral hemorrhage (ICH) in rats. Male Wistar rats were divided into 8 groups of 10 according the stroke type induced: Sham IR, Sham IR+GT, IR, IR+GT, Sham ICH, Sham ICH+GT, ICH, ICH+GT. Supplementation with GT was initiated 10days before stroke surgery and continuous for 6days after (GT dose 400mg/kg). Short (STM) and long term memory (LTM) we evaluated with object recognition task (OR) and hippocampus were used to evaluate parameters related to oxidative stress (ROS, lipid peroxidation and total antioxidant capacity). The rats subjected to IR and ICH showed STM and LTM deficits and GT intervention prevented it in both stroke models. IR and ICH induced increase on ROS levels in hippocampus. ICH increased the lipid peroxidation in hippocampus and the GT supplementation avoided it. IR induced decrease on total antioxidant capacity and GT prevented it. These results reveal that GT supplementation presents a neuroprotective role, attenuates redox imbalance and might have a beneficial impact on cognitive function after stroke.

Effects of green tea and physical exercise on memory impairments associated with aging.

We investigated the effects of physical exercise and green tea supplementation (associated or not) on biochemical and behavioral parameters in the time course of normal aging. Male Wistar rats aged 9 months were divided into groups: control, physical exercise (treadmill running), and supplemented with green tea while either performing physical exercise or not. A young control group was also studied. Physical exercise and green tea supplementation lasted 3 months. Afterwards, behavioral and biochemical tests were performed. Biochemical measurements revealed differences in antioxidant and oxidant responses in hippocampus, prefrontal cortex and striatum. Behavioral testing showed age-related memory impairments reversed by physical exercise. The association of green tea supplementation and physical exercise did not provide aged rats with additional improvements in memory or brain oxidative markers. Green tea per se significantly decreased reactive oxygen species levels and improved antioxidant defenses although it did not reverse memory deficits associated with normal aging.

Memory deficits and oxidative stress in cerebral ischemia-reperfusion: neuroprotective role of physical exercise and green tea supplementation.

Ischemic stroke is a major cause of morbidity and mortality all over the world. Among impairments observed in survivors there is a significant cognitive learning and memory deficit. Neuroprotective strategies are being investigated to minimize such deficits after an ischemia event. Here we investigated the neuroprotective potential of physical exercise and green tea in an animal model of ischemia-reperfusion. Eighty male rats were divided in 8 groups and submitted to either transient brain ischemia-reperfusion or a sham surgery after 8 weeks of physical exercise and/or green tea supplementation. Ischemia-reperfusion was performed by bilateral occlusion of the common carotid arteries during 30 min. Later, their memory was evaluated in an aversive and in a non-aversive task, and hippocampus and prefrontal cortex were removed for biochemical analyses of possible oxidative stress effects. Ischemia-reperfusion impaired learning and memory. Reactive oxygen species were increased in the hippocampus and prefrontal cortex. Eight weeks of physical exercise and/or green tea supplementation before the ischemia-reperfusion event showed a neuroprotective effect; both treatments in separate or together reduced the cognitive deficits and were able to maintain the functional levels of antioxidant enzymes and glutathione.