Maísa Corrêa

Resveratrol prevents memory deficits and the increase in acetylcholinesterase activity in streptozotocin-induced diabetic rats

The objective of the present study was to investigate the effect of the administration of resveratrol (RV) on memory and on acetylcholinesterase (AChE) activity in the cerebral cortex, hippocampus, striatum, hypothalamus, cerebellum and blood in streptozotocin-induced diabetic rats. The animals were divided into six groups (n=6-13): Control/saline; Control/RV 10 mg/kg; Control/RV 20 mg/kg; Diabetic/saline; Diabetic/RV 10 mg/kg; Diabetic/RV 20 mg/kg. One day after 30 days of treatment with resveratrol the animals were submitted to behavioral tests and then submitted to euthanasia and the brain structures and blood were collected. The results showed a decrease in step-down latency in diabetic/saline group. Resveratrol (10 and 20 mg/kg) prevented the impairment of memory induced by diabetes. In the open field test, no significant differences were observed between the groups. In relation to AChE activity, a significant increase in diabetic/saline group (P<0.05) was observed in all brain structures compared to control/saline group. However, AChE activity decreased significantly in control/RV10 and control/RV20 (P<0.05) groups in cerebral cortex, hippocampus and striatum, while no significant differences were observed in diabetic/RV10 and diabetic/RV20 groups in all brain structures compared to control/saline group. Blood AChE activity increased significantly in diabetic/saline group (P<0.05) decreased in control/RV10, control/RV20 and diabetic/RV20 groups (P<0.05) compared to control/saline group. In conclusion, the present findings showed that treatment with resveratrol prevents the increase in AChE activity and consequently memory impairment in diabetic rats, demonstrating that this compound can modulate cholinergic neurotransmission and consequently improve cognition.

Pre-treatment with ebselen and vitamin E modulate acetylcholinesterase activity: interaction with demyelinating agents

The ethidium bromide (EB) demyelinating model was associated with vitamin E (Vit E) and ebselen (Ebs) treatment to evaluate acetylcholinesterase (AChE) activity in the striatum (ST), hippocampus (HP), cerebral cortex (CC) and erythrocytes. Rats were divided into seven groups: I—Control (saline), II—(canola); III—(Ebs), IV—(Vit E); V—(EB); VI—(EB + Ebs) and VII—(EB + Vit E). At 3 days after the EB injection, AChE activity in the CC and HC was significantly reduced in groups III, IV, V, VI and VII (p < 0.05) and in the ST it was reduced in groups III and V (p < 0.05) when compared to the control group. At 21 days after the EB injection, AChE activity in the CC was significantly reduced in groups III, IV and V, while in groups VI and VII a significant increase was observed when compared to the control group. In the HC and ST, AChE activity was significantly reduced in groups V, VI and VII when compared to the control group (p < 0.05). In the erythrocytes, at 3 days after the EB injection, AChE activity was significantly reduced in groups III, IV, V, VI and VII and at 21 days there was a significant reduction only in groups VI and VII (p < 0.05) when compared to the control group. In conclusion, this study demonstrated that Ebs and Vit E interfere with the cholinergic neurotransmission by altering AChE activity in the different brain regions and in the erythrocytes. Furthermore, treatment with Vit E and Ebs protected against the demyelination lesion caused by EB. In this context, we can suggest that ebselen and Vit E should be considered potential therapeutics and scientific tools to be investigated in brain disorders associated with demyelinating events.

The activity and expression of NTPDase is altered in lymphocytes of multiple sclerosis patients

BACKGROUND Multiple sclerosis (MS) is a demyelinating neurological disease, which is presumed to be a consequence of infiltrating lymphocytes that are autoreactive to myelin proteins. ATP and adenosine contribute to fine-tuning immune responses and NTPDase (CD39) and adenosine deaminase (ADA) are important enzymes in the control of the extracellular levels of these molecules at the site of inflammation. We evaluated the activity and expression of NTPDase and adenosine deaminase (ADA) activity in lymphocytes from patients with the relapsing-remitting form of MS (RRMS). METHODS This study involved 22 patients with RRMS and 22 healthy subjects as a control group. The lymphocytes were isolated from blood and separated on Ficoll density gradients and after isolation the NTPDase and ADA activities were determined. RESULTS The NTPDase activity and expression were increased in lymphocytes from RRMS patients when compared with the control group (p<0.05). In addition, a decrease in ADA activity was observed in lymphocytes from these patients when compared to the control group (p<0.05). CONCLUSIONS The regulation of ATP and adenosine levels by NTPDase and ADA activities may be important to preserve cellular integrity and to modulate the immune response in MS.

Influence of malathion on acetylcholinesterase activity in rats submitted to a forced swimming test

The organophosphorus insecticides, including malathion, are used indiscriminately in large amounts, causing environmental pollution and risk to human health. Classically, this toxicity is attributed mainly to the accumulation of acetylcholine (ACh), due inhibition of acetylcholinesterase (AChE), and consequently overstimulation of the nicotinic and muscarinic receptors. The present study investigated the effects of acute and chronic malathion administration in immobility time in the forced swimming test (FST), openfield test and AChE activity in neural tissue of rats. Malathion was administered intraperitoneally once a day for one day (acute) or for 28 days (chronic) (in both protocols malathion was administered at 25, 50, 100 and 150 mg/kg). No significant effect was seen in immobility time in the FST after acute malathion treatment. The chronic malathion treatment induced an increase in the time of immobility in the FST. Both treatments do not interfere in locomotor activity evaluated in a novel environment. The inhibition of AChE activity was significant in the hippocampus (25, 50, 100 and 150 mg/kg), cortex (100 and 150 mg/ kg) and striatum (150 mg/kg) after chronic treatment, but not significantly after acute treatment. These data suggest a possible interaction between increased immobility time in the FST and activation of cholinergic receptors by accumulated ACh subsequent to AChE inhibition.