Rosa MM

References (4)

Title : Neuroprotective effects of quercetin on memory and anxiogenic-like behavior in diabetic rats: Role of ectonucleotidases and acetylcholinesterase activities - Maciel_2016_Biomed.Pharmacother_84_559
Author(s) : Maciel RM , Carvalho FB , Olabiyi AA , Schmatz R , Gutierres JM , Stefanello N , Zanini D , Rosa MM , Andrade CM , Rubin MA , Schetinger MR , Morsch VM , Danesi CC , Lopes ST
Ref : Biomed Pharmacother , 84 :559 , 2016
Abstract : The present study investigated the protective effect of quercetin (Querc) on memory, anxiety-like behavior and impairment of ectonucleotidases and acetylcholinesterase (AChE) activities in brain of streptozotocin-induced diabetic rats (STZ-diabetes). The type 1 diabetes mellitus was induced by an intraperitoneal injection of 70mg/kg of streptozotocin (STZ), diluted in 0.1M sodium-citrate buffer (pH 4.5). Querc was dissolved in 25% ethanol and administered by gavage at the doses of 5, 25 and 50mg/kg once a day during 40days. The animals were distributed in eight groups of ten animals as follows: vehicle, Querc 5mg/kg, Querc 25mg/kg, Querc 50mg/kg, diabetes, diabetes plus Querc 5mg/kg, diabetes plus Querc 25mg/kg and diabetes plus Querc 50mg/kg. Querc was able to prevent the impairment of memory and the anxiogenic-like behavior induced by STZ-diabetes. In addition, Querc prevents the decrease in the NTPDase and increase in the adenosine deaminase (ADA) activities in SN from cerebral cortex of STZ-diabetes. STZ-diabetes increased the AChE activity in SN from cerebral cortex and hippocampus. Querc 50mg/kg was more effective to prevent the increase in AChE activity in the brain of STZ-diabetes. Querc also prevented an increase in the malondialdehyde levels in all the brain structures. In conclusion, the present findings showed that Querc could prevent the impairment of the enzymes that regulate the purinergic and cholinergic extracellular signaling and improve the memory and anxiety-like behavior induced by STZ-diabetes.
ESTHER : Maciel_2016_Biomed.Pharmacother_84_559
PubMedSearch : Maciel_2016_Biomed.Pharmacother_84_559
PubMedID: 27694000

Title : Quercetin protects the impairment of memory and anxiogenic-like behavior in rats exposed to cadmium: Possible involvement of the acetylcholinesterase and Na,K-ATPase activities - Abdalla_2014_Physiol.Behav_135C_152
Author(s) : Abdalla FH , Schmatz R , Cardoso AM , Carvalho FB , Baldissarelli J , de Oliveira JS , Rosa MM , Goncalves Nunes MA , Rubin MA , da Cruz IB , Barbisan F , Dressler VL , Pereira LB , Schetinger MR , Morsch VM , Goncalves JF , Mazzanti CM
Ref : Physiol Behav , 135C :152 , 2014
Abstract : The present study investigated the effects of quercetin in the impairment of memory and anxiogenic-like behavior induced by cadmium (Cd) exposure. We also investigated possible alterations in acetylcholinesterase (AChE), Na+,K+-ATPase and delta-aminolevulinate dehydratase (delta-ALA-D) activities as well as in oxidative stress parameters in the CNS. Rats were exposed to Cd (2.5mg/kg) and quercetin (5, 25 or 50mg/kg) by gavage for 45days. Animals were divided into eight groups (n=10-14): saline/control, saline/Querc 5mg/kg, saline/Querc 25mg/kg, saline/Querc 50mg/kg, Cd/ethanol, Cd/Querc 5mg/kg, Cd/Querc 25mg/kg and Cd/Querc 50mg/kg. Results demonstrated that Cd impaired memory has an anxiogenic effect. Quercetin prevented these harmful effects induced by Cd. AChE activity decreased in the cerebral cortex and hippocampus and increased in the hypothalamus of Cd-exposed rats. The Na+,K+-ATPase activity decreased in the cerebral cortex, hippocampus and hypothalamus of Cd-exposed rats. Quercetin prevented these effects in AChE and Na+,K+-ATPase activities. Reactive oxygen species production, thiobarbituric acid reactive substance levels, protein carbonyl content and double-stranded DNA fractions increased in the cerebral cortex, hippocampus and hypothalamus of Cd-exposed rats. Quercetin totally or partially prevents these effects caused by Cd. Total thiols (T-SHs), reduced glutathione (GSH), and reductase glutathione (GR) activities decreased and glutathione S-transferase (GST) activity increased in Cd exposed rats. Co-treatment with quercetin prevented reduction in T-SH, GSH, and GR activities and the rise of GST activity. The present findings show that quercetin prevents alterations in oxidative stress parameters as well as AChE and Na+,K+-ATPase activities, consequently preventing memory impairment and anxiogenic-like behavior displayed by Cd exposure. These results may contribute to a better understanding of the neuroprotective role of quercetin, emphasizing the influence of this flavonoid in the diet for human health, possibly preventing brain injury associated with Cd intoxication.
ESTHER : Abdalla_2014_Physiol.Behav_135C_152
PubMedSearch : Abdalla_2014_Physiol.Behav_135C_152
PubMedID: 24952260

Title : Neuroprotective effect of anthocyanins on acetylcholinesterase activity and attenuation of scopolamine-induced amnesia in rats - Gutierres_2013_Int.J.Dev.Neurosci_33C_88
Author(s) : Gutierres JM , Carvalho FB , Schetinger MR , Agostinho P , Marisco PC , Vieira JM , Rosa MM , Bohnert C , Rubin MA , Morsch VM , Spanevello R , Mazzanti CM
Ref : Int J Developmental Neuroscience , 33C :88 , 2013
Abstract : Anthocyanins are a group of natural phenolic compounds responsible for the color to plants and fruits. These compounds might have beneficial effects on memory and have antioxidant properties. In the present study we have investigated the therapeutic efficacy of anthocyanins in an animal model of cognitive deficits, associated to Alzheimer's disease, induced by scopolamine. We evaluated whether anthocyanins protect the effects caused by SCO on nitrite/nitrate (NOx) levels and Na+,K+-ATPase and Ca2+-ATPase and acetylcholinesterase (AChE) activities in the cerebral cortex and hippocampus (of rats. We used 4 different groups of animals: control (CTRL), anthocyanins treated (ANT), scopolamine-challenged (SCO), and scopolamine+anthocyanins (SCO+ANT). After seven days of treatment with ANT (200mgkg-1; oral), the animals were SCO injected (1mgkg-1; IP) and were performed the behavior tests, and submitted to euthanasia. A memory deficit was found in SCO group, but ANT treatment prevented this impairment of memory (P<0.05). The ANT treatment per se had an anxiolytic effect. AChE activity was increased in both in cortex and hippocampus of SCO group, this effect was significantly attenuated by ANT (P<0.05). SCO decreased Na+,K+-ATPase and Ca2+-ATPase activities in hippocampus, and ANT was able to significantly (P<0.05) prevent these effects. No significant alteration was found on NOx levels among the groups. In conclusion, the ANT is able to regulate cholinergic neurotransmission and restore the Na+,K+-ATPase and Ca2+-ATPase activities, and also prevented memory deficits caused by scopolamine administration.
ESTHER : Gutierres_2013_Int.J.Dev.Neurosci_33C_88
PubMedSearch : Gutierres_2013_Int.J.Dev.Neurosci_33C_88
PubMedID: 24374256

Title : Rivastigmine for dementia associated with Parkinson's disease - Emre_2004_N.Engl.J.Med_351_2509
Author(s) : Emre M , Aarsland D , Albanese A , Byrne EJ , Deuschl G , De Deyn PP , Durif F , Kulisevsky J , van Laar T , Lees A , Poewe W , Robillard A , Rosa MM , Wolters E , Quarg P , Tekin S , Lane R
Ref : N Engl J Med , 351 :2509 , 2004
Abstract : BACKGROUND: Cholinergic deficits are prominent in patients who have dementia associated with Parkinson's disease. We investigated the effects of the dual cholinesterase inhibitor rivastigmine in such patients.
METHODS: Patients in whom mild-to-moderate dementia developed at least 2 years after they received a clinical diagnosis of Parkinson's disease were randomly assigned to receive placebo or 3 to 12 mg of rivastigmine per day for 24 weeks. Primary efficacy variables were the scores for the cognitive subscale of the Alzheimer's Disease Assessment Scale (ADAS-cog) and Alzheimer's Disease Cooperative Study-Clinician's Global Impression of Change (ADCS-CGIC). Secondary clinical outcomes were the scores for the Alzheimer's Disease Cooperative Study-Activities of Daily Living, the 10-item Neuropsychiatric Inventory, the Mini-Mental State Examination, Cognitive Drug Research power of attention tests, the Verbal Fluency test, and the Ten Point Clock-Drawing test.
RESULTS: A total of 541 patients were enrolled, and 410 completed the study. The outcomes were better among patients treated with rivastigmine than among those who received placebo; however, the differences between these two groups were moderate and similar to those reported in trials of rivastigmine for Alzheimer's disease. Rivastigmine-treated patients had a mean improvement of 2.1 points in the score for the 70-point ADAS-cog, from a baseline score of 23.8, as compared with a 0.7-point worsening in the placebo group, from a baseline score of 24.3 (P<0.001). Clinically meaningful improvements in the scores for the ADCS-CGIC were observed in 19.8 percent of patients in the rivastigmine group and 14.5 percent of those in the placebo group, and clinically meaningful worsening was observed in 13.0 percent and 23.1 percent, respectively (mean score at 24 weeks, 3.8 and 4.3, respectively; P=0.007). Significantly better outcomes were seen with rivastigmine with respect to all secondary efficacy variables. The most frequent adverse events were nausea (affecting 29.0 percent of patients in the rivastigmine group and 11.2 percent of those in the placebo group, P<0.001), vomiting (16.6 and 1.7 percent, P<0.001), and tremor (10.2 and 3.9 percent, P=0.01).
CONCLUSIONS: In this placebo-controlled study, rivastigmine was associated with moderate improvements in dementia associated with Parkinson's disease but also with higher rates of nausea, vomiting, and tremor.
ESTHER : Emre_2004_N.Engl.J.Med_351_2509
PubMedSearch : Emre_2004_N.Engl.J.Med_351_2509
PubMedID: 15590953