Carvalho FB

References (21)

Title : Effect of QTC-4-MeOBnE Treatment on Memory, Neurodegeneration, and Neurogenesis in a Streptozotocin-Induced Mouse Model of Alzheimer's Disease - Fronza_2021_ACS.Chem.Neurosci_12_109
Author(s) : Fronza MG , Baldinotti R , Sacramento M , Gutierres J , Carvalho FB , Fernandes MDC , Sousa FSS , Seixas FK , Collares T , Alves D , Pratico D , Savegnago L
Ref : ACS Chem Neurosci , 12 :109 , 2021
Abstract : Growing evidence suggests that drugs targeting neurogenesis and myelinization could be novel therapeutic targets against Alzheimer's disease (AD). Intracerebroventricular (icv) injection of streptozotocin (STZ) induces neurodegeneration through multiple mechanisms ultimately resulting in reduced adult neurogenesis. Previously, the multitarget compound QTC-4-MeOBnE (1-(7-chloroquinolin-4-yl)-N-(4-methoxybenzyl)-5-methyl-1H-1,2,3-triazole-4-carboxamide) demonstrated beneficial effects in preclinical models of AD. Here we investigated its pharmacokinetics profile and the effect on memory impairments and neurodegeneration induced by STZ. Two icv injections of STZ resulted in significant cognitive and memory impairments, assessed by novel object recognition, Y-maze, social recognition, and step-down passive avoidance paradigms. These deficits were reversed in STZ-injected mice treated with QTC-4-MeOBnE. This effect was associated with reversion of neuronal loss in hippocampal dentate gyrus, reduced oxidative stress, and amelioration of synaptic function trough Na(+)/K(+) ATPase and acetylcholinesterase activities. Furthermore, brains from QTC-4-MeOBnE-treated mice had a significant increase in adult neurogenesis and remyelination through Prox1/NeuroD1 and Wnt/beta-catenin pathways. Overall, our findings support the potential anti-AD effect of QTC-4-MeOBnE through multiple pathways, all of which have been involved in the onset and progression of the disease.
ESTHER : Fronza_2021_ACS.Chem.Neurosci_12_109
PubMedSearch : Fronza_2021_ACS.Chem.Neurosci_12_109
PubMedID: 33315382

Title : Protective Effects of Inosine on Memory Consolidation in a Rat Model of Scopolamine-Induced Cognitive Impairment: Involvement of Cholinergic Signaling, Redox Status, and Ion Pump Activities - Teixeira_2021_Neurochem.Res__
Author(s) : Teixeira FC , de Mattos BDS , Mello JE , Cardoso J , Spohr L , Luduvico KP , Soares MSP , Carvalho FB , Gutierres JM , Oliveira Campello Felix A , Stefanello FM , Spanevello RM
Ref : Neurochem Res , : , 2021
Abstract : This study investigated the effects of inosine on memory acquisition and consolidation, cholinesterases activities, redox status and Na(+), K(+)-ATPase activity in a rat model of scopolamine-induced cognitive impairment. Adult male rats were divided into four groups: control (saline), scopolamine (1 mg/kg), scopolamine plus inosine (50 mg/kg), and scopolamine plus inosine (100 mg/kg). Inosine was pre-administered for 7 days, intraperitoneally. On day 8, scopolamine was administered pre (memory acquisition protocol) or post training (memory consolidation protocol) on inhibitory avoidance tasks. The animals were subjected to the step-down inhibitory avoidance task 24 hours after the training. Scopolamine induced impairment in the acquisition and consolidation phases; however, inosine was able to prevent only the impairment in memory consolidation. Also, scopolamine increased the activity of acetylcholinesterase and reduced the activity of Na(+), K(+)-ATPase and the treatment with inosine protected against these alterations in consolidation protocol. In the animals treated with scopolamine, inosine improved the redox status by reducing the levels of reactive oxygen species and thiobarbituric acid reactive substances and restoring the activity of the antioxidant enzymes, superoxide dismutase and catalase. Our findings suggest that inosine may offer protection against scopolamine-induced memory consolidation impairment by modulating brain redox status, cholinergic signaling and ion pump activity. This compound may provide an interesting approach in pharmacotherapy and as a prophylactic against neurodegenerative mechanisms involved in Alzheimer's disease.
ESTHER : Teixeira_2021_Neurochem.Res__
PubMedSearch : Teixeira_2021_Neurochem.Res__
PubMedID: 34623562

Title : Hypermethioninemia induces memory deficits and morphological changes in hippocampus of young rats: implications on pathogenesis - Soares_2020_Amino.Acids__
Author(s) : Soares MSP , de Mattos BDS , de Souza AA , Spohr L , Tavares RG , Siebert C , Moreira DS , Wyse ATS , Carvalho FB , Rahmeier F , Fernandes MDC , Stefanello FM , Spanevello RM
Ref : Amino Acids , : , 2020
Abstract : The aim of this study was to investigate the effect of the chronic administration of methionine (Met) and/or its metabolite, methionine sulfoxide (MetO), on the behavior and neurochemical parameters of young rats. Rats were treated with saline (control), Met (0.2-0.4 g/kg), MetO (0.05-0.1 g/kg), and/or a combination of Met + MetO, subcutaneously twice a day from postnatal day 6 (P6) to P28. The results showed that Met, MetO, and Met + MetO impaired short-term and spatial memories (P < 0.05), reduced rearing and grooming (P < 0.05), but did not alter locomotor activity (P > 0.05). Acetylcholinesterase activity was increased in the cerebral cortex, hippocampus, and striatum following Met and/or MetO (P < 0.05) treatment, while Na(+), K(+)-ATPase activity was reduced in the hippocampus (P < 0.05). There was an increase in the level of thiobarbituric acid reactive substances (TBARS) in the cerebral cortex in Met-, MetO-, and Met + MetO-treated rats (P < 0.05). Met and/or MetO treatment reduced superoxide dismutase, catalase, and glutathione peroxidase activity, total thiol content, and nitrite levels, and increased reactive oxygen species and TBARS levels in the hippocampus and striatum (P < 0.05). Hippocampal brain-derived neurotrophic factor was reduced by MetO and Met + MetO compared with the control group. The number of NeuN-positive cells was decreased in the CA3 in Met + MetO group and in the dentate gyrus in the Met, MetO, and Met + MetO groups compared to control group (P < 0.05). Taken together, these findings further increase our understanding of changes in the brain in hypermethioninemia by elucidating behavioral alterations, biological mechanisms, and the vulnerability of brain function to high concentrations of Met and MetO.
ESTHER : Soares_2020_Amino.Acids__
PubMedSearch : Soares_2020_Amino.Acids__
PubMedID: 31902007

Title : Quercetin treatment regulates the Na(+),K(+)-ATPase activity, peripheral cholinergic enzymes, and oxidative stress in a rat model of demyelination - Carvalho_2018_Nutr.Res_55_45
Author(s) : Carvalho FB , Gutierres JM , Beckmann D , Santos RP , Thome GR , Baldissarelli J , Stefanello N , Andrades A , Aiello G , Ripplinger A , Lucio BM , Ineu R , Mazzanti A , Morsch V , Schetinger MR , Andrade CM
Ref : Nutr Res , 55 :45 , 2018
Abstract : Quercetin is reported to exert a plethora of health benefits through many different mechanisms of action. This versatility and presence in the human diet has attracted the attention of the scientific community, resulting in a huge output of in vitro and in vivo (preclinical) studies. Therefore, we hypothesized that quercetin can protect Na(+),K(+)-ATPase activity in the central nervous system, reestablish the peripheral cholinesterases activities, and reduce oxidative stress during demyelination events in rats. In line with this expectation, our study aims to find out how quercetin acts on the Na(+),K(+)-ATPase activity in the central nervous system, peripheral cholinesterases, and stress oxidative markers in an experimental model of demyelinating disease. Wistar rats were divided into 4 groups: vehicle, quercetin, ethidium bromide (EB), and EB plus quercetin groups. The animals were treated once a day with vehicle (ethanol 20%) or quercetin 50 mg/kg for 7 (demyelination phase, by gavage) or 21 days (remyelination phase) after EB (0.1%, 10 muL) injection (intrapontine).The encephalon was removed, and the pons, hypothalamus, cerebral cortex, hippocampus, striatum, and cerebellum were dissected to verify the Na(+),K(+)-ATPase activity. Our results showed that quercetin protected against reduction in Na(+),K(+)-ATPase in the pons and cerebellum in the demyelination phase, and it increased the activity of this enzyme in the remyelination phase. During the demyelination, quercetin promoted the increase in acetylcholinesterase activity in whole blood and lymphocytes induced by EB, and it reduced the increase in acetylcholinesterase activity in lymphocytes in the remyelination phase. On day 7, EB increased the superoxide dismutase and decreased catalase activities, as well as increased the thiobarbituric acid-reactive substance levels. Taken together, these results indicated that quercetin regulates the Na(+),K(+)-ATPase activity, affects the alterations of redox state, and participates in the reestablishment of peripheral cholinergic activity during demyelinating and remyelination events.
ESTHER : Carvalho_2018_Nutr.Res_55_45
PubMedSearch : Carvalho_2018_Nutr.Res_55_45
PubMedID: 29914627

Title : Dietary supplementation of tiger nut alters biochemical parameters relevant to erectile function in l-NAME treated rats - Olabiyi_2018_Food.Res.Int_109_358
Author(s) : Olabiyi AA , Carvalho FB , Bottari NB , Lopes TF , da Costa P , Stefanelo N , Morsch VM , Akindahunsi AA , Oboh G , Schetinger MR
Ref : Food Res Int , 109 :358 , 2018
Abstract : Tiger nut tubers have been reportedly used for the treatment of erectile dysfunction (ED) in folk medicine without scientific basis. Hence, this study evaluated the effect of tiger nut on erectile dysfunction by assessing biochemical parameters relevant to ED in male rats by nitric oxide synthase (NOS) inhibitor, Nomega-nitro-l-arginine methyl ester hydrochloride (l-NAME) treatment. Rats were divided into five groups (n=10) each: Control group; l-NAME plus basal diet; l-NAME plus Sildenafil citrate; diet supplemented processed tiger nut (20%) plus l-NAME;diet supplemented raw tiger nut (20%) plus l-NAME. l-NAME pre-treatment (40mg/kg/day) lasted for 14days. Arginase, acetycholinesterase (AChE) and adenosine deaminase (ADA) activities as well as nitric oxide levels (NO) in serum, brain and penile tissue were measured. l-NAME increased the activity of arginase, AChE and ADA and reduced NO levels. However, dietary supplementation with tiger nut caused a reduction on the activities of the above enzymes and up regulated nitric oxide levels when compared to the control group. The effect of tiger nut supplemented diet may be said to prevent alterations of the activities of the enzymes relevant in erectile function. Quercetin was revealed to be the most active component of tiger nut tuber by HPLC finger printing.
ESTHER : Olabiyi_2018_Food.Res.Int_109_358
PubMedSearch : Olabiyi_2018_Food.Res.Int_109_358
PubMedID: 29803461

Title : Caffeine and high intensity exercise: Impact on purinergic and cholinergic signalling in lymphocytes and on cytokine levels - Vieira_2018_Biomed.Pharmacother_108_1731
Author(s) : Vieira JM , Gutierres JM , Carvalho FB , Stefanello N , Oliveira L , Cardoso AM , Morsch VM , Pillat MM , Ulrich H , Duarte MMF , Schetinger MRC , Spanevello RM
Ref : Biomed Pharmacother , 108 :1731 , 2018
Abstract : This study evaluated the effects of caffeine in combination with high-intensity interval training (HIIT) on sensitivity to glucocorticoids and proliferation of lymphocytes, IL-6 and IL-10 levels and NTPDase, adenosine deaminase (ADA) and acetylcholinesterase (AChE) activity in rat lymphocytes. The animals were divided into groups: control, caffeine 4 mg/kg, caffeine 8 mg/kg, HIIT, HIIT plus caffeine 4 mg/kg and HIIT plus caffeine 8 mg/kg. The rats were trained three times a week for 6 weeks for a total workload 23% of body weight at the end of the experiment. Caffeine was administered orally 30 min before the training session. When lymphocytes were stimulated with phytohaemagglutinin no changes were observed in proliferative response between trained and sedentary animals; however, when caffeine was associated with HIIT an increase in T lymphocyte proliferation and in the sensitivity of lymphocytes to glucocorticoids occurred. ATP and ADP hydrolysis was decreased in the lymphocytes of the animals only trained and caffeine treatment prevented alterations in ATP hydrolysis. HIIT caused an increase in the ADA and AChE activity in lymphocytes and this effect was more pronounced in rats trained and supplemented with caffeine. The level of IL-6 was increased while the level of IL-10 was decreased in trained animals (HIIT) and caffeine was capable of preventing this exercise effect. Our findings suggest that caffeine ingestion attenuates, as least in part, the immune and inflammatory alterations following a prolonged HIIT protocol.
ESTHER : Vieira_2018_Biomed.Pharmacother_108_1731
PubMedSearch : Vieira_2018_Biomed.Pharmacother_108_1731
PubMedID: 30372876

Title : Anthocyanins as a potential pharmacological agent to manage memory deficit, oxidative stress and alterations in ion pump activity induced by experimental sporadic dementia of Alzheimer's type - Pacheco_2018_J.Nutr.Biochem_56_193
Author(s) : Pacheco SM , Soares MSP , Gutierres JM , Gerzson MFB , Carvalho FB , Azambuja JH , Schetinger MRC , Stefanello FM , Spanevello RM
Ref : J Nutr Biochem , 56 :193 , 2018
Abstract : Anthocyanins (ANT) are polyphenolic flavonoids with antioxidant and neuroprotective properties. This study evaluated the effect of ANT treatment on cognitive performance and neurochemical parameters in an experimental model of sporadic dementia of Alzheimer's type (SDAT). Adult male rats were divided into four groups: control (1 ml/kg saline, once daily, by gavage), ANT (200 mg/kg, once daily, by gavage), streptozotocin (STZ, 3 mg/kg) and STZ plus ANT. STZ was administered via bilateral intracerebroventricular (ICV) injection (5 mul). ANT were administered after ICV injection for 25 days. Cognitive deficits (short-term memory and spatial memory), oxidative stress parameters, and acetylcholinesterase (AChE) and Na(+)-K(+)-ATPase activity in the cerebral cortex and hippocampus were evaluated. ANT treatment protected against the worsening of memory in STZ-induced SDAT. STZ promoted an increase in AChE and Na(+)-K(+)-ATPase total and isoform activity in both structures; ANT restored this change. STZ administration induced an increase in lipid peroxidation and decrease in the level of antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), in the cerebral cortex; ANT significantly attenuated these effects. In the hippocampus, an increase in reactive oxygen species (ROS), nitrite and lipid peroxidation levels, and SOD activity and a decrease in CAT and GPx activity were seen after STZ injection. ANT protected against the changes in ROS and antioxidant enzyme levels. In conclusion, the present study showed that treatment with ANT attenuated memory deficits, protected against oxidative damage in the brain, and restored AChE and ion pump activity in an STZ-induced SDAT in rats.
ESTHER : Pacheco_2018_J.Nutr.Biochem_56_193
PubMedSearch : Pacheco_2018_J.Nutr.Biochem_56_193
PubMedID: 29587242

Title : Southern Brazilian native fruit shows neurochemical, metabolic and behavioral benefits in an animal model of metabolic syndrome - Oliveira_2018_Metab.Brain.Dis_33_1551
Author(s) : Oliveira PS , Chaves VC , Soares MSP , Bona NP , Mendonca LT , Carvalho FB , Gutierres JM , Vasconcellos FA , Vizzotto M , Vieira A , Spanevello RM , Reginatto FH , Lencina CL , Stefanello FM
Ref : Metabolic Brain Disease , 33 :1551 , 2018
Abstract : In this work, we evaluated the effects of Psidium cattleianum (Red Type) (PcRT) fruit extract on metabolic, behavioral, and neurochemical parameters in rats fed with a highly palatable diet (HPD) consisted of sucrose (65% carbohydrates being 34% from condensed milk, 8% from sucrose and 23% from starch, 25% protein and 10% fat). Animals were divided into 4 groups: standard chow, standard chow + PcRT extract (200 mg/Kg/day by gavage), HPD, HPD + extract. The animals were treated for 150 days. Concerning chemical profiling, LC/PDA/MS/MS analysis revealed cyanidin-3-O-glucoside as the only anthocyanin in the PcRT extract. Our results showed that the animals exposed to HPD presented glucose intolerance, increased weight gain and visceral fat, as well as higher serum levels of glucose, triacylglycerol, total cholesterol, LDL-cholesterol and interleukin-6. These alterations were prevented by PcRT. In addition, HPD caused an increase in immobility time in a forced swimming test and the fruit extract prevented this alteration, indicating an antidepressant-like effect. PcRT treatment also prevented increased acetylcholinesterase activity in the prefrontal cortex caused by HPD consumption. Moreover, PcRT extract was able to restore Ca(2+)-ATPase activity in the prefrontal cortex, hippocampus, and striatum, as well as Na(+),K(+)-ATPase activity in the prefrontal cortex and hippocampus. PcRT treatment decreased thiobarbituric acid-reactive substances, nitrite, and reactive oxygen species levels and prevented the reduction of superoxide dismutase activity in all cerebral structures of the HPD group. Additionally, HPD decreased catalase in the hippocampus and striatum. However, the extract prevented this change in the hippocampus. Our results showed that this berry extract has antihyperglycemic and antihyperlipidemic effects, and neuroprotective properties, proving to be a potential therapeutic agent for individuals with metabolic syndrome.
ESTHER : Oliveira_2018_Metab.Brain.Dis_33_1551
PubMedSearch : Oliveira_2018_Metab.Brain.Dis_33_1551
PubMedID: 29882020

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 : A comparative study of the effect of the dose and exposure duration of anabolic androgenic steroids on behavior, cholinergic regulation, and oxidative stress in rats - Bueno_2017_PLoS.One_12_e0177623
Author(s) : Bueno A , Carvalho FB , Gutierres JM , Lhamas C , Andrade CM
Ref : PLoS ONE , 12 :e0177623 , 2017
Abstract : The aim of this study was to assess if the dose and exposure duration of the anabolic androgenic steroids (AAS) boldenone (BOL) and stanazolol (ST) affected memory, anxiety, and social interaction, as well as acetylcholinesterase (AChE) activity and oxidative stress in the cerebral cortex (CC) and hippocampus (HC). Male Wistar rats (90 animals) were randomly assigned to three treatment protocols: (I) 5 mg/kg BOL or ST, once a week for 4 weeks; (II) 2.5 mg/kg BOL or ST, once a week for 8 weeks; and (III) 1.25 mg/kg BOL or ST, once a week for 12 weeks. Each treatment protocol included a control group that received an olive oil injection (vehicle control) and AAS were administered intramuscularly (a total volume of 0.2 ml) once a week in all three treatment protocols. In the BOL and ST groups, a higher anxiety level was observed only for Protocol I. BOL and ST significantly affected social interaction in all protocols. Memory deficits and increased AChE activity in the CC and HC were found in the BOL groups treated according to Protocol III only. In addition, BOL and ST significantly increased oxidative stress in both the CC and HC in the groups treated according to Protocol I and III. In conclusion, our findings show that the impact of BOL and ST on memory, anxiety, and social interaction depends on the dose and exposure duration of these AAS.
ESTHER : Bueno_2017_PLoS.One_12_e0177623
PubMedSearch : Bueno_2017_PLoS.One_12_e0177623
PubMedID: 28594925

Title : Caffeine prevents changes in muscle caused by high-intensity interval training - Vieira_2017_Biomed.Pharmacother_89_116
Author(s) : Vieira JM , Gutierres JM , Carvalho FB , Pereira LB , Oliveira LS , Morsch VM , Schetinger MR , Rodrigues MV , Leitemperger J , Loro V , Krewer CC , Vencato MS , Spanevello RM
Ref : Biomed Pharmacother , 89 :116 , 2017
Abstract : The use of ergogenic substances such as caffeine has become a strategy to enhance sports performance. In the present study we evaluated the effects of high-intensity interval training (HIIT) associated with caffeine intake on acetylcholinesterase (AChE) and Ca2+ATPase activity and glycogen levels in the muscles of rats were evaluated. The animals were divided in groups: control, caffeine 4 or 8mg/kg, HIIT, HIIT plus caffeine 4 or caffeine 8mg/kg. Our results showed a decrease in glycogen levels in muscle in all trained groups after acute session exercise, while that an increase in glycogen levels was observed in all groups in relation to control in chronic exercise protocol. HIIT increases the thickness of the left ventricle and the Ca2+-ATPase activity and decrease the AChE activity in gastrocnemius muscle. Caffeine treatment prevents changes in enzymes activities as well as left ventricular hypertrophy adaptation induced by HIIT. Our findings suggest that caffeine modulates crucial pathways for muscle contraction in HIIT.
ESTHER : Vieira_2017_Biomed.Pharmacother_89_116
PubMedSearch : Vieira_2017_Biomed.Pharmacother_89_116
PubMedID: 28222393

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 : Cholinesterases as markers of the inflammatory process associated oxidative stress in cattle infected by Babesia bigemina - Doyle_2016_Comp.Immunol.Microbiol.Infect.Dis_46_1
Author(s) : Doyle RL , Da Silva AS , Oliveira CB , Franca RT , Carvalho FB , Abdalla FH , Costa P , Klafke GM , Martins JR , Tonin AA , Castro VS , Santos FG , Lopes ST , Andrade CM
Ref : Comp Immunol Microbiol Infect Dis , 46 :1 , 2016
Abstract : The objective of this study was to assess the influence of an asymptomatic experimental infection by Babesia bigemina on cholinesterase's as markers of the inflammatory process and biomarkers of oxidative imbalance. For this purpose, eight naive animals were used, as follows: four as controls or uninfected; and four infected with an attenuated strain of B. bigemina. Blood samples were collected on days 0, 7 and 11 post-inoculation (PI). Parasitemia was determined by blood smear evaluation, showing that the infection by B. bigemina resulted in mean 0.725 and 0.025% on day 7 and 11 PI, respectively, as well as mild anemia. The activities of acetylcholinesterase, butyrylcholinesterase and catalase were lower, while levels of thiobarbituric acid reactive substances and superoxide dismutase activity were higher in infected animals, when compared with the control group. This attenuated strain of B. bigemina induced an oxidative stress condition, as well as it reduces the cholinesterases activity in infected and asymptomatic cattle. Therefore, this decrease of cholinesterase in infection by B. bigemina purpose is to inhibit inflammation, for thereby increasing acetylcholine levels, potent anti-inflammatory molecules.
ESTHER : Doyle_2016_Comp.Immunol.Microbiol.Infect.Dis_46_1
PubMedSearch : Doyle_2016_Comp.Immunol.Microbiol.Infect.Dis_46_1
PubMedID: 27260803

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 : Neuroprotective role of quercetin in locomotor activities and cholinergic neurotransmission in rats experimentally demyelinated with ethidium bromide - Beckmann_2014_Life.Sci_103_79
Author(s) : Beckmann DV , Carvalho FB , Mazzanti CM , Dos Santos RP , Andrades AO , Aiello G , Rippilinger A , Graca DL , Abdalla FH , Oliveira LS , Gutierres JM , Schetinger MR , Mazzanti A
Ref : Life Sciences , 103 :79 , 2014
Abstract : AIM: The purpose of this study was to investigate whether the flavonoid quercetin can prevent alterations in the behavioral tests and of cholinergic neurotransmission in rats submitted to the ethidium bromide (EB) experimental demyelination model during events of demyelination and remyelination. MAIN
METHODS: Wistar rats were randomly distributed into four groups (20 animals per group): Control (pontine saline injection and treatment with ethanol), Querc (pontine saline injection and treatment with quercetin), EB (pontine 0.1% EB injection and treatment with ethanol), and EB+Querc (pontine 0.1% EB injection and treatment with quercetin). The groups Querc and Querc+EB were treated once daily with quercetin (50mg/kg) diluted in 25% ethanol solution (1ml/kg) and the animals of the control and EB groups were treated once daily with 25% ethanol solution (1ml/kg). Two stages were observed: phase of demyelination (peak on day 7) and phase of remyelination (peak on day 21 post-injection). Behavioral tests (beam walking, foot fault and inclined plane test), acetylcholinesterase (AChE) activity and lipid peroxidation in pons, cerebellum, hippocampus, hypothalamus, striatum and cerebral cortex were measured. KEY FINDINGS: The quercetin promoted earlier locomotor recovery, suggesting that there was demyelination prevention or further remyelination velocity as well as it was able to prevent the inhibition of AChE activity and the increase of lipidic peroxidation, suggesting that this compound can protect cholinergic neurotransmission. SIGNIFICANCE: These results may contribute to a better understanding of the neuroprotective role of quercetin and the importance of an antioxidant diet in humans to provide benefits in neurodegenerative diseases such as MS.
ESTHER : Beckmann_2014_Life.Sci_103_79
PubMedSearch : Beckmann_2014_Life.Sci_103_79
PubMedID: 24727240

Title : Parkia biglobosa Improves Mitochondrial Functioning and Protects against Neurotoxic Agents in Rat Brain Hippocampal Slices - Komolafe_2014_Biomed.Res.Int_2014_326290
Author(s) : Komolafe K , Olaleye TM , Seeger RL , Carvalho FB , Boligon AA , Athayde ML , Klimaczewski CV , Akindahunsi AA , Rocha JB
Ref : Biomed Res Int , 2014 :326290 , 2014
Abstract : Objective. Methanolic leaf extracts of Parkia biglobosa, PBE, and one of its major polyphenolic constituents, catechin, were investigated for their protective effects against neurotoxicity induced by different agents on rat brain hippocampal slices and isolated mitochondria. Methods. Hippocampal slices were preincubated with PBE (25, 50, 100, or 200 microg/mL) or catechin (1, 5, or 10 microg/mL) for 30 min followed by further incubation with 300 microM H2O2, 300 microM SNP, or 200 microM PbCl2 for 1 h. Effects of PBE and catechin on SNP- or CaCl2-induced brain mitochondrial ROS formation and mitochondrial membrane potential (DeltaPsim) were also determined. Results. PBE and catechin decreased basal ROS generation in slices and blunted the prooxidant effects of neurotoxicants on membrane lipid peroxidation and nonprotein thiol contents. PBE rescued hippocampal cellular viability from SNP damage and caused a significant boost in hippocampus Na(+), K(+)-ATPase activity but with no effect on the acetylcholinesterase activity. Both PBE and catechin also mitigated SNP- or CaCl2-dependent mitochondrial ROS generation. Measurement by safranine fluorescence however showed that the mild depolarization of the DeltaPsim by PBE was independent of catechin. Conclusion. The results suggest that the neuroprotective effect of PBE is dependent on its constituent antioxidants and mild mitochondrial depolarization propensity.
ESTHER : Komolafe_2014_Biomed.Res.Int_2014_326290
PubMedSearch : Komolafe_2014_Biomed.Res.Int_2014_326290
PubMedID: 25177688

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