The present study investigated the effects of resveratrol (RV), a polyphenol with potent antioxidant properties, on oxidative stress parameters in liver and kidney, as well as on serum biochemical parameters of streptozotocin (STZ)-induced diabetic rats. Animals were divided into six groups (n = 8): control/saline; control/RV 10 mg/kg; control/RV 20 mg/kg; diabetic/saline; diabetic/RV10 mg/kg; diabetic/RV 20 mg/kg. After 30 days of treatment with resveratrol the animals were sacrificed and the liver, kidney and serum were used for experimental determinations. Results showed that TBARS levels were significantly increased in the diabetic/saline group and the administration of resveratrol prevented this increase in the diabetic/RV10 and diabetic/RV20 groups (P < 0.05). The activities of catalase (CAT), superoxide dismutase (SOD) and aminolevulinic acid dehydratase (δ-ALA-D) and the levels of non protein thiols (NPSH) and vitamin C presented a significant decrease in the diabetic/saline group when compared with the control/saline group (P < 0.05). The treatment with resveratrol was able to prevent these decrease improving the antioxidant defense of the diabetic/RV10 and diabetic/RV20 groups (P < 0.05). In addition, the elevation in serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and γ-glutamiltransferase (γ-GT) activities as well as in levels of urea, creatinine, cholesterol and triglycerides observed in the diabetic/saline group were reverted to levels close to normal by the administration of resveratrol in the diabetic/RV10 and diabetic/RV20 groups (P < 0.05). These findings suggest that resveratrol could have a protector effect against hepatic and renal damage induced by oxidative stress in the diabetic state, which was evidenced by the capacity of this polyphenol to modulate the antioxidant defense and to decrease the lipid peroxidation in these tissues.

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Acetylcholinesterase (AChE) is distributed throughout the body in both neuronal and non-neuronal tissues and plays an important role in the regulation of physiological events. Caffeic acid is a phenolic compound that has anti-inflammatory and neuroprotective properties. The aim of this study was to investigate in vitro and in vivo whether caffeic acid alters the AChE activity and behavioral parameters in rats. In the in vitro study, the concentrations of 0, 0.1, 0.5, 1.0, 1.5, and 2mM of caffeic acid were used. For the in vivo study, five groups were evaluated: group I (control); group II (canola oil), group III (10mg/kg of caffeic acid); group IV (50mg/kg of caffeic acid) and group V (100mg/kg of caffeic acid). Caffeic acid was diluted in canola oil and administered for 30 days. In vitro, the caffeic acid increased the AChE activity in the cerebral cortex, cerebellum, hypothalamus, whole blood, and lymphocytes at different concentrations. In muscle, this compound caused an inhibition in the AChE activity at concentrations of 0.5, 1.0, 1.5, and 2mM when compared to the control (P<0.05). In vivo, 50 and 100mg/kg of caffeic acid decreased the AChE activity in the cerebral cortex and striatum and increased the activity of this enzyme in the cerebellum, hippocampus, hypothalamus, pons, lymphocytes, and muscles when compared to the control group (P<0.05). The amount of 100mg/kg of caffeic acid improved the step-down latencies in the inhibitory avoidance. Our results demonstrated that caffeic acid improved memory and interfered with the cholinergic signaling. As a natural and promising compound caffeic acid should be considered potentially therapeutic in disorders that involve the cholinergic system.

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In conclusion, these findings demonstrated that ANT is able to regulate ion pump activity and cholinergic neurotransmission, as well as being able to enhance memory and act as an anxiolytic compound in animals with SDAT.