Rubin MA

References (14)

Title : Curcumin attenuates memory deficits and the impairment of cholinergic and purinergic signaling in rats chronically exposed to cadmium - da Costa_2017_Environ.Toxicol_32_70
Author(s) : da Costa P , Goncalves JF , Baldissarelli J , Mann TR , Abdalla FH , Fiorenza AM , da Rosa MM , Carvalho FB , Gutierres JM , de Andrade CM , Rubin MA , Schetinger MR , Morsch VM
Ref : Environ Toxicol , 32 :70 , 2017
Abstract : This study investigated the protective effect of curcumin on memory loss and on the alteration of acetylcholinesterase and ectonucleotidases activities in rats exposed chronically to cadmium (Cd). Rats received Cd (1 mg/kg) and curcumin (30, 60, or 90 mg/kg) by oral gavage 5 days a week for 3 months. The animals were divided into eight groups: vehicle (saline/oil), saline/curcumin 30 mg/kg, saline/curcumin 60 mg/kg, saline/curcumin 90 mg/kg, Cd/oil, Cd/curcumin 30 mg/kg, Cd/curcumin 60 mg/kg, and Cd/curcumin 90 mg/kg. Curcumin prevented the decrease in the step-down latency induced by Cd. In cerebral cortex synaptosomes, Cd-exposed rats showed an increase in acetylcholinesterase and NTPDase (ATP and ADP as substrates) activities and a decrease in the 5'-nucleotidase activity. Curcumin was not able to prevent the effect of Cd on acetylcholinesterase activity, but it prevented the effects caused by Cd on NTPDase (ATP and ADP as substrate) and 5'-nucleotidase activities. Increased acetylcholinesterase activity was observed in different brain structures, whole blood and lymphocytes of the Cd-treated group. In addition, Cd increased lipid peroxidation in different brain structures. Higher doses of curcumin were more effective in preventing these effects. These findings show that curcumin prevented the Cd-mediated memory impairment, demonstrating that this compound has a neuroprotective role and is capable of modulating acetylcholinesterase, NTPDase, and 5'-nucleotidase activities. Finally, it highlights the possibility of using curcumin as an adjuvant against toxicological conditions involving Cd exposure. (c) 2015 Wiley Periodicals, Inc. Environ Toxicol 32: 70-83, 2017.
ESTHER : da Costa_2017_Environ.Toxicol_32_70
PubMedSearch : da Costa_2017_Environ.Toxicol_32_70
PubMedID: 26592365

Title : Neuroprotective effects of pretreatment with quercetin as assessed by acetylcholinesterase assay and behavioral testing in poloxamer-407 induced hyperlipidemic rats - Braun_2017_Biomed.Pharmacother_88_1054
Author(s) : Braun JB , Ruchel JB , Adefegha SA , Coelho AP , Trelles KB , Signor C , Rubin MA , Oliveira JS , Dornelles GL , de Andrade CM , Castilhos LG , Leal DB
Ref : Biomed Pharmacother , 88 :1054 , 2017
Abstract : Hyperlipidemia is a group of disorders characterized by excessive lipids in the bloodstream. It is associated with the incidence of cardiovascular diseases and recognized as the most important factor underlying the occurrence of atherosclerosis. This study was conducted to investigate whether pretreatment with quercetin can protect against possible memory impairment and deterioration of the cholinergic system in hyperlipidemic rats. Animals were divided into ten groups (n=7): saline/control, saline/quercetin 5mg/kg, saline/quercetin 25mg/kg, saline/quercetin 50mg/kg, saline/simvastatin (0.04mg/kg), hyperlipidemia, hyperlipidemia/quercetin 5mg/kg, hyperlipidemia/quercetin 25mg/kg, hyperlipidemia/quercetin 50mg/kg and hyperlipidemia/simvastatin. The animals were pretreated with quercetin by oral gavage for a period of 30days and hyperlipidemia was subsequently induced by intraperitoneal administration of a single dose of 500mg/kg of poloxamer-407. Simvastatin was administered after the induction of hyperlipidemia. The results demonstrated that hyperlipidemic rats had memory impairment compared with the saline control group (P<0.001). However, pretreatment with quercetin and simvastatin treatment attenuated the damage caused by hyperlipidemia compared with the hyperlipidemic group (P<0.05). Acetylcholinesterase (AChE) activity in the cerebral hippocampus was significantly (P<0.001) reduced in the hyperlipidemic group compared with the control saline group. Pretreatment with quercetin and simvastatin treatment in the hyperlipidemic groups significantly (P<0.05) increased AChE activity compared with the hyperlipidemic group. Our results thus suggest that quercetin may prevent memory impairment, alter lipid metabolism, and modulate AChE activity in an experimental model of hyperlipidemia.
ESTHER : Braun_2017_Biomed.Pharmacother_88_1054
PubMedSearch : Braun_2017_Biomed.Pharmacother_88_1054
PubMedID: 28192878

Title : Berberine protects against memory impairment and anxiogenic-like behavior in rats submitted to sporadic Alzheimer's-like dementia: Involvement of acetylcholinesterase and cell death - de Oliveira_2016_Neurotoxicol_57_241
Author(s) : de Oliveira JS , Abdalla FH , Dornelles GL , Adefegha SA , Palma TV , Signor C , da Silva Bernardi J , Baldissarelli J , Lenz LS , Magni LP , Rubin MA , Pillat MM , de Andrade CM
Ref : Neurotoxicology , 57 :241 , 2016
Abstract : The present study aimed to investigate the effects of berberine (BRB) on spatial and learning memory, anxiety, acetylcholinesterase activity and cell death in an experimental model of intracerebroventricular streptozotocin (ICV-STZ) induced sporadic Alzheimer's-like dementia. Sixty male Wistar rats were randomly divided into six groups: control (CTR), BRB 50mg/kg (BRB 50), BRB 100mg/kg (BRB 100), streptozotocin (STZ), streptozotocin plus BRB 50mg/kg (STZ+BRB 50), and streptozotocin plus BRB 100mg/kg (STZ+BRB 100). Rats were injected with ICV-STZ (3mg/kg) or saline, and daily oral BRB treatment began on day 4 for a period of 21days. Behavioral tests were carried out on day 17, and rats were euthanized on day 24. Cell death analysis and determination of acetylcholinesterase activity was performed on the cerebral cortex and hippocampus of the brain. Administration of BRB prevented the memory loss, anxiogenic behavior, increased acetylcholinesterase activity and cell death induced by ICV-STZ. This may be explained, in part, by a protective effect of BRB on ameliorating the progression of neurodegenerative diseases, including Alzheimer's disease, and the results of this study provide a better understanding of the effect of BRB on the brain. Thus, BRB may act as a potential neuroprotective agent.
ESTHER : de Oliveira_2016_Neurotoxicol_57_241
PubMedSearch : de Oliveira_2016_Neurotoxicol_57_241
PubMedID: 27746125

Title : Guarana (Paullinia cupana) ameliorates memory impairment and modulates acetylcholinesterase activity in Poloxamer-407-induced hyperlipidemia in rat brain - Ruchel_2016_Physiol.Behav_168_11
Author(s) : Ruchel JB , Braun JB , Adefegha SA , Guedes Manzoni A , Abdalla FH , de Oliveira JS , Trelles K , Signor C , Lopes ST , da Silva CB , Castilhos LG , Rubin MA , Leal DB
Ref : Physiol Behav , 168 :11 , 2016
Abstract : Hyperlipidemia is a risk factor for the development of cognitive dysfunction and atherosclerosis. Natural compounds have recently received special attention in relation to the treatment of disease due to their low cost and wide margin of safety. Thus, the aim of this study was to determine the possible preventive effect of guarana powder (Paullinia cupana) on memory impairment and acetylcholinesterase (AChE) activity in the brain structures of rats with Poloxamer-407-induced hyperlipidemia. Adult male Wistar rats were pretreated with guarana (12.5, 25 and 50mg/kg/day) and caffeine (0.2mg/kg/day) by gavage for a period of 30days. Simvastatin (0.04mg/kg) was administered as a comparative standard. Acute hyperlipidemia was induced with intraperitoneal injections of 500mg/kg of Poloxamer-407. Memory tests and evaluations of anxiety were performed. The cortex, cerebellum, hippocampus, hypothalamus and striatum were separated to assess acetylcholinesterase activity. Our results revealed that guarana powder was able to reduce the levels of TC and LDL-C in a manner similar to simvastatin. Guarana powder also partially reduced the liver damage caused by hyperlipidemia. Guarana was able to prevent changes in the activity of AChE and improve memory impairment due to hyperlipidemia. Guarana powder may therefore be a source of promising phytochemicals that can be used as adjuvant therapy in the management of hyperlipidemia and cognitive disorders.
ESTHER : Ruchel_2016_Physiol.Behav_168_11
PubMedSearch : Ruchel_2016_Physiol.Behav_168_11
PubMedID: 27720901

Title : Diphenyl diselenide supplementation in infected mice by Toxoplasma gondii: Protective effect on behavior, neuromodulation and oxidative stress caused by disease - Machado_2016_Exp.Parasitol_169_51
Author(s) : Machado VS , Bottari NB , Baldissera MD , Rech VC , Ianiski FR , Signor C , Rubin MA , Waczuk EP , Schwertz CI , Mendes RE , Camillo G , Vogel FF , de La Rue ML , Morsch VM , Schetinger MR , Fruhauf PK , Da Silva AS
Ref : Experimental Parasitology , 169 :51 , 2016
Abstract : The aim of this study was to evaluate the effect of subcutaneous administration of diphenyl diselenide (PhSe)2 on animal behavior and activities of acetylcholinesterase (AChE), adenylate kinase (AK), and creatine kinase (CK) in the brain of mice infected by Toxoplasma gondii. In addition, thiobarbituric acid reactive species (TBARS) levels and glutathione (GR, GPx and GST) activity were also evaluated. For the study, 40 female mice were divided into four groups of 10 animals each: group A (uninfected and untreated), group B (uninfected and treated with (PhSe)2), group C (infected and untreated) and group D (infected and treated with (PhSe)2). The mice were inoculated with 50 cysts of the ME49 strain of T. gondii. After infection the animals of the groups B and D were treated on days 1 and 20 post-infection (PI) with 5.0 mumol/kg of (PhSe)2 subcutaneously. Behavioral tests were conducted on days 29 PI to assess memory loss (object recognition), anxiety (elevated plus maze), locomotor and exploratory activity (Open Field) and it was found out that infected and untreated animals (group C) had developed anxiety and memory impairment, and the (PhSe)2 treatment did not reverse these behavioral changes on infected animals treated with (PhSe)2 (group D). The results showed an increase on AChE activity (P < 0.01) in the brain of infected and untreated animals (group C) compared to the uninfected and untreated animals (group A). The AK and CK activities decreased in infected and untreated animals (group C) compared to the uninfected and untreated animals (group A) (P < 0.01), however the (PhSe)2 treatment did not reverse these alterations. Infected and untreated animals (group C) showed increased TBARS levels and GR activity, and decreased GPx and GST activities when compared to uninfected and untreated animals (group A). Infected animals treated with (PhSe)2 (group D) decreased TBARS levels and GR activity, while increased GST activity when compared to infected and untreated animals (group C). It was concluded that (PhSe)2 showed antioxidant activity, but the dose used had no anti-inflammatory effect and failed to reverse the behavioral changes caused by the parasite.
ESTHER : Machado_2016_Exp.Parasitol_169_51
PubMedSearch : Machado_2016_Exp.Parasitol_169_51
PubMedID: 27472985

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 : Anthocyanins restore behavioral and biochemical changes caused by streptozotocin-induced sporadic dementia of Alzheimer's type - Gutierres_2014_Life.Sci_96_7
Author(s) : Gutierres JM , Carvalho FB , Schetinger MR , Marisco P , Agostinho P , Rodrigues M , Rubin MA , Schmatz R , da Silva CR , de PCG , Farias JG , Signor C , Morsch VM , Mazzanti CM , Bogo M , Bonan CD , Spanevello R
Ref : Life Sciences , 96 :7 , 2014
Abstract : AIMS: The aim of this study was to analyze if the pre-administration of anthocyanin on memory and anxiety prevented the effects caused by intracerebroventricular streptozotocin (icv-STZ) administration-induced sporadic dementia of Alzheimer's type (SDAT) in rats. Moreover, we evaluated whether the levels of nitrite/nitrate (NOx), Na(+),K(+)-ATPase, Ca(2+)-ATPase and acethylcholinesterase (AChE) activities in the cerebral cortex (CC) and hippocampus (HC) are altered in this experimental SDAT. MAIN
METHODS: Male Wistar rats were divided in 4 different groups: control (CTRL), anthocyanin (ANT), streptozotocin (STZ) and streptozotocin+anthocyanin (STZ+ANT). After seven days of treatment with ANT (200mg/kg; oral), the rats were icv-STZ injected (3mg/kg), and four days later the behavior parameters were performed and the animals submitted to euthanasia. KEY FINDINGS: A memory deficit was found in the STZ group, but ANT treatment showed that it prevents this impairment of memory (P<0.05). Our results showed a higher anxiety in the icv-STZ group, but treatment with ANT showed a per se effect and prevented the anxiogenic behavior induced by STZ. Our results reveal that the ANT treatment (100muM) tested displaces the specific binding of [(3)H] flunitrazepam to the benzodiazepinic site of GABAA receptors. AChE, Ca(+)-ATPase activities and NOx levels were found to be increased in HC and CC in the STZ group, which was attenuated by ANT (P<0.05). STZ decreased Na(+),K(+)-ATPase activity and ANT was able to prevent these effects (P<0.05). SIGNIFICANCE: 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.
ESTHER : Gutierres_2014_Life.Sci_96_7
PubMedSearch : Gutierres_2014_Life.Sci_96_7
PubMedID: 24291256

Title : Effect of vitamin D3 on behavioural and biochemical parameters in diabetes type 1-induced rats - Calgaroto_2014_Cell.Biochem.Funct_32_502
Author(s) : Calgaroto NS , Thome GR , da Costa P , Baldissareli J , Hussein FA , Schmatz R , Rubin MA , Signor C , Ribeiro DA , Carvalho FB , de Oliveira LS , Pereira LB , Morsch VM , Schetinger MR
Ref : Cell Biochemistry & Function , 32 :502 , 2014
Abstract : Diabetes is associated with long-term complications in the brain and reduced cognitive ability. Vitamin D3 (VD3 ) appears to be involved in the amelioration of hyperglycaemia in streptozotocin (STZ)-induced diabetic rats. Our aim was to analyse the potential of VD3 in avoiding brain damage through evaluation of acetylcholinesterase (AChE), Na(+) K(+) -adenosine triphosphatase (ATPase) and delta aminolevulinate dehydratase (delta-ALA-D) activities and thiobarbituric acid reactive substance (TBARS) levels from cerebral cortex, as well as memory in STZ-induced diabetic rats. Animals were divided into eight groups (n = 5): control/saline, control/metformin (Metf), control/VD3 , control/Metf + VD3 , diabetic/saline, diabetic/Metf, diabetic/VD3 and diabetic/Metf + VD3 . Thirty days after treatment, animals were submitted to contextual fear-conditioning and open-field behavioural tests, after which they were sacrificed and the cerebral cortex was dissected. Our results demonstrate a significant memory deficit, an increase in AChE activity and TBARS levels and a decrease in delta-ALA-D and Na(+) K(+) -ATPase activities in diabetic rats when compared with the controls. Treatment of diabetic rats with Metf and VD3 prevented the increase in AChE activity when compared with the diabetic/saline group. In treated diabetic rats, the decrease in Na(+) K(+) -ATPase was reverted when compared with non-treated rats, but the increase in delta-ALA-D activity was not. VD3 prevented diabetes-induced TBARS level and improved memory. Our results show that VD3 can avoid cognitive deficit through prevention of changes in important enzymes such as Na(+) K(+) -ATPase and AChE in cerebral cortex in type 1 diabetic rats. Copyright (c) 2014 John Wiley & Sons, Ltd.
ESTHER : Calgaroto_2014_Cell.Biochem.Funct_32_502
PubMedSearch : Calgaroto_2014_Cell.Biochem.Funct_32_502
PubMedID: 24947461

Title : Effects of chlorogenic acid, caffeine, and coffee on behavioral and biochemical parameters of diabetic rats - Stefanello_2014_Mol.Cell.Biochem_388_277
Author(s) : Stefanello N , Schmatz R , Pereira LB , Rubin MA , da Rocha JB , Facco G , Pereira ME , Mazzanti CM , Passamonti S , Rodrigues MV , Carvalho FB , da Rosa MM , Gutierres JM , Cardoso AM , Morsch VM , Schetinger MR
Ref : Molecular & Cellular Biochemistry , 388 :277 , 2014
Abstract : Diabetes mellitus (DM) is associated with brain alterations that may contribute to cognitive dysfunctions. Chlorogenic acid (CGA) and caffeine (CA), abundant in coffee (CF), are natural compounds that have showed important actions in the brain. The present study aimed to evaluate the effect of CGA, CA, and CF on acetylcholinesterase (AChE), Na(+), K(+)-ATPase, aminolevulinate dehydratase (delta-ALA-D) activities and TBARS levels from cerebral cortex, as well as memory and anxiety in streptozotocin-induced diabetic rats. Animals were divided into eight groups (n = 5-10): control; control/CGA 5 mg/kg; control/CA 15 mg/kg; control/CF 0.5 g/kg; diabetic; diabetic/CGA 5 mg/kg; diabetic/CA 15 mg/kg; and diabetic/CF 0.5 g/kg. Our results demonstrated an increase in AChE activity and TBARS levels in cerebral cortex, while delta-ALA-D and Na(+), K(+)-ATPase activities were decreased in the diabetic rats when compared to control water group. Furthermore, a memory deficit and an increase in anxiety in diabetic rats were observed. The treatment with CGA and CA prevented the increase in AChE activity in diabetic rats when compared to the diabetic water group. CGA, CA, and CF intake partially prevented cerebral delta-ALA-D and Na(+), K(+)-ATPase activity decrease due to diabetes. Moreover, CGA prevented diabetes-induced TBARS production, improved memory, and decreased anxiety. In conclusion, among the compounds studied CGA proved to be a compound which acts better in the prevention of brain disorders promoted by DM.
ESTHER : Stefanello_2014_Mol.Cell.Biochem_388_277
PubMedSearch : Stefanello_2014_Mol.Cell.Biochem_388_277
PubMedID: 24370728

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 : Effects of caffeic acid on behavioral parameters and on the activity of acetylcholinesterase in different tissues from adult rats - Anwar_2012_Pharmacol.Biochem.Behav_103_386
Author(s) : Anwar J , Spanevello RM , Thome G , Stefanello N , Schmatz R , Gutierres J , Vieira J , Baldissarelli J , Carvalho FB , da Rosa MM , Rubin MA , Fiorenza A , Morsch VM , Schetinger MR
Ref : Pharmacol Biochem Behav , 103 :386 , 2012
Abstract : 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 30days. 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.
ESTHER : Anwar_2012_Pharmacol.Biochem.Behav_103_386
PubMedSearch : Anwar_2012_Pharmacol.Biochem.Behav_103_386
PubMedID: 22982740

Title : N-acetylcysteine prevents memory deficits, the decrease in acetylcholinesterase activity and oxidative stress in rats exposed to cadmium - Goncalves_2010_Chem.Biol.Interact_186_53
Author(s) : Goncalves JF , Fiorenza AM , Spanevello RM , Mazzanti CM , Bochi GV , Antes FG , Stefanello N , Rubin MA , Dressler VL , Morsch VM , Schetinger MR
Ref : Chemico-Biological Interactions , 186 :53 , 2010
Abstract : The present study investigated the effect of the administration of N-acetylcysteine (NAC), on memory, on acetylcholinesterase (AChE) activity and on lipid peroxidation in different brain structures in cadmium (Cd)-exposed rats. The rats received Cd (2 mg/kg) and NAC (150 mg/kg) by gavage every other day for 30 days. The animals were divided into four groups (n=12-13): control/saline, NAC, Cd, and Cd/NAC. The results showed a decrease in step-down latency in the Cd-group, but NAC reversed the impairment of memory induced by Cd intoxication. Rats exposed to Cd and/or treated with NAC did not demonstrate altered shock sensitivity. Decreased AChE activity was found in hippocampus, cerebellum and hypothalamus in the Cd-group but NAC reversed this effect totally or partially while in cortex synaptosomes and striatum there was no alteration in AChE activity. An increase in TBARS levels was found in hippocampus, cerebellum and hypothalamus in the Cd-group and NAC abolished this effect while in striatum there was no alteration in TBARS levels. Urea and creatinine levels were increased in serum of Cd-intoxicated rats, but NAC was able to abolish these undesirable effects. The present findings show that treatment with NAC prevented the Cd-mediated decrease in AChE activity, as well as oxidative stress and consequent memory impairment in Cd-exposed rats, demonstrating that this compound may modulate cholinergic neurotransmission and consequently improve cognition. However, it is necessary to note that the mild renal failure may be a contributor to the behavioral impairment found in this investigation.
ESTHER : Goncalves_2010_Chem.Biol.Interact_186_53
PubMedSearch : Goncalves_2010_Chem.Biol.Interact_186_53
PubMedID: 20399762

Title : Resveratrol prevents memory deficits and the increase in acetylcholinesterase activity in streptozotocin-induced diabetic rats - Schmatz_2009_Eur.J.Pharmacol_610_42
Author(s) : Schmatz R , Mazzanti CM , Spanevello R , Stefanello N , Gutierres J , Correa M , da Rosa MM , Rubin MA , Chitolina Schetinger MR , Morsch VM
Ref : European Journal of Pharmacology , 610 :42 , 2009
Abstract : 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.
ESTHER : Schmatz_2009_Eur.J.Pharmacol_610_42
PubMedSearch : Schmatz_2009_Eur.J.Pharmacol_610_42
PubMedID: 19303406