Mazzanti A

References (9)

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 : 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 : 17-beta estradiol in the acetylcholinesterase activity and lipid peroxidation in the brain and blood of ovariectomized adult and middle-aged rats - Martins_2012_Life.Sci_90_351
Author(s) : Martins DB , Mazzanti CM , Franca RT , Pagnoncelli M , Costa MM , de Souza EM , Goncalves J , Spanevello R , Schmatz R , da Costa P , Mazzanti A , Beckmann DV , Cecim Mda S , Schetinger MR , Lopes ST
Ref : Life Sciences , 90 :351 , 2012
Abstract : AIMS: To investigate the 17-beta estradiol in the acetylcholinesterase activity and lipid peroxidation in the brain and blood of ovariectomized rats of different ages. MAIN METHODS: Animals were randomly assigned into three experimental groups of each age (n=6). Control groups consisted of adult (sham-A) and middle-aged (sham-MA) female rats, ovariectomized adult (OVX-A) and middle-aged (OVX-MA) rats without estrogen therapy reposition, and ovariectomized adult (OVX+E2-A) and middle-aged (OVX+E2-MA) rats treated with 17-beta estradiol for 30days. After this period, AChE activity and lipid peroxidation were measured in the brain and blood. KEY FINDINGS: The AChE activity increased (p<0.05) in striatum (ST) in OVX-A, OVX+E2-A and OVX-MA, and hippocampus (HP) in OVX-MA. The enzyme activity decreased (p<0.05) in ST of OVX+E2-MA, and cerebral cortex (CC) in OVX+E2-A, OVX-MA and OVX+E2-MA. Blood AChE activity increased (p<0.05) in OVX+E2-A and decreased (p<0.05) in OVX-MA. Lymphocyte AChE activity increased (p<0.05) in OVX-A and OVX+E2-A and decreased (p<0.05) in OVX-MA. Lipid peroxidation increased (p<0.05) in ST of OVX-A, CC of OVX-A and OVX-MA, HP of OVX-A, and cerebellum (CE) of OVX-A, OVX-MA, and OVX+E2-MA. Lipid peroxidation decreased (p<0.05) in ST, CC and CE of OVX+E2-A, and ST and HP of OVX+E2-MA. Similar values of lipid peroxidation to control groups were found in ST and HP of OVX-MA, HP of OVX+E2-A and CC of OVX+E2-MA. SIGNIFICANCE: 17-beta estradiol is able to modulate the AChE activity and non-neuronal cholinergic response as well as to reduce lipid peroxidation. Its response is dependent on the age and brain structure analyzed.
ESTHER : Martins_2012_Life.Sci_90_351
PubMedSearch : Martins_2012_Life.Sci_90_351
PubMedID: 22227472

Title : Diphenyl diselenide ameliorates cognitive deficits induced by a model of menopause in rats - da Rocha_2012_Behav.Pharmacol_23_98
Author(s) : da Rocha JT , Pinton S , Mazzanti A , Mazzanti CM , Beckemann DV , Nogueira CW , Zeni G
Ref : Behav Pharmacol , 23 :98 , 2012
Abstract : Ovarian hormone loss contributes to cognitive decline in postmenopausal women. Studies have demonstrated a positive role of the level of the element selenium in cognitive performance. The present study investigated the effects of the synthetic organoselenium compound diphenyl diselenide (PhSe)(2) on cognitive functions in ovariectomized rats. Ninety-day-old female Wistar rats were subjected to ovariectomy (OVX) or Sham operation. One week after surgery, rats were orally treated with (PhSe)(2) (5 mg/kg, per oral route) or vehicle once a day for 30 days. Next, the rats were evaluated in behavioral tests [Morris water maze (MWM) and open-field tests] and biochemical [cerebral acetylcholinesterase (AChE)] analyses were carried out. In MWM probe trial, (PhSe)(2) decreased the latency to reach the platform location and increased the number of crossings over the platform location, protecting against cognitive impairment induced by OVX. Furthermore, (PhSe)(2) prevented the stimulation of AChE activity caused by OVX. In conclusion, the present study showed a cognition-enhancing effect of (PhSe)(2) treatment for 30 days in ovariectomized rats in the MWM test, which could be related to its ability to prevent the stimulation of AChE activity caused by OVX in rats. These findings suggest that (PhSe)(2) might have a promising role in preventing the cognitive decline related to menopause.
ESTHER : da Rocha_2012_Behav.Pharmacol_23_98
PubMedSearch : da Rocha_2012_Behav.Pharmacol_23_98
PubMedID: 22139607

Title : Vitamin E decreased the activity of acetylcholinesterase and level of lipid peroxidation in brain of rats exposed to aged and diluted sidestream smoke - Thome_2011_Nicotine.Tob.Res_13_1210
Author(s) : Thome GR , Spanevello RM , Mazzanti A , Fiorenza AM , Duarte MM , da Luz SC , Pereira ME , Morsch VM , Schetinger MR , Mazzanti CM
Ref : Nicotine Tob Res , 13 :1210 , 2011
Abstract : INTRODUCTION: The biological systems of both smoker and passive smoking suffer changes caused by toxic compounds from cigarette smoke such as inflammation, lipid peroxidation, and deficiency of vitamin E. The aim of the present study was to evaluate the effect of vitamin E on acetylcholinesterase (AChE) activity and the lipid peroxidation level in the brain of rats in the model of exposure to aged and diluted sidestream smoke (ADSS). METHODS: Adult male Wistar rats (200-300 g) were exposed to ADSS for 4 weeks and treated with vitamin E (50 mg/kg/day) loaded by gavage. In the first, second, third, and fourth weeks, animals were concomitantly exposed to the smoke of 1, 2, 3, and 4 cigarettes/day, respectively. The duration of each exposure was 15 min, daily. RESULTS: For rats exposed to ADSS, the AChE activity and lipid peroxidation level increased in the striatum, cerebral cortex, and cerebellum. In contrast, the activity of AChE and the level of lipid peroxidation decreased in the smoke group treated with vitamin E. CONCLUSIONS: The results suggest that the rats exposed to ADSS and treated with vitamin E significantly reduced the raised activity of AChE and level lipid peroxidation from the brain structures studied. The study, therefore, concludes that vitamin E could be considered as a therapeutic agent in this type of exposure.
ESTHER : Thome_2011_Nicotine.Tob.Res_13_1210
PubMedSearch : Thome_2011_Nicotine.Tob.Res_13_1210
PubMedID: 21896885

Title : Pre-treatment with ebselen and vitamin E modulate acetylcholinesterase activity: interaction with demyelinating agents - Mazzanti_2009_Int.J.Dev.Neurosci_27_73
Author(s) : Mazzanti CM , Spanevello R , Ahmed M , Pereira LB , Goncalves JF , Correa M , Schmatz R , Stefanello N , Leal DB , Mazzanti A , Ramos AT , Martins TB , Danesi CC , Graca DL , Morsch VM , Schetinger MR
Ref : Int J Developmental Neuroscience , 27 :73 , 2009
Abstract : 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.
ESTHER : Mazzanti_2009_Int.J.Dev.Neurosci_27_73
PubMedSearch : Mazzanti_2009_Int.J.Dev.Neurosci_27_73
PubMedID: 18930802

Title : Cyclosporine A inhibits acetylcholinesterase activity in rats experimentally demyelinated with ethidium bromide - Mazzanti_2007_Int.J.Dev.Neurosci_25_259
Author(s) : Mazzanti CM , Spanevello R , Ahmed M , Schmatz R , Mazzanti A , Salbego FZ , Graca DL , Sallis ES , Morsch VM , Schetinger MR
Ref : Int J Developmental Neuroscience , 25 :259 , 2007
Abstract : Cyclosporine A is the major immunosuppressive agent used for organ transplantation and for the treatment of a variety of autoimmune disorders such as multiple sclerosis. In this work, we investigated the effect of the cyclosporine A on the acetylcholinesterase activity in the cerebral cortex, striatum, hippocampus, hypothalamus, cerebellum and pons of the rats experimentally demyelinated by ethidium bromide. Rats were divided into four groups: I control (injected with saline), II (treated with cyclosporine A), III (injected with 0.1% ethidium bromide) and IV (injected with 0.1% the ethidium bromide and treated with cyclosporine A). The results showed a significant inhibition (p<0.05) of acetylcholinesterase activity in the groups II, III and IV in all brain structures analyzed. In the striatum, hippocampus, hypothalamus and pons the inhibition was greater (p<0.005) when ethidium bromide was associated with cyclosporine A. In conclusion, the present investigation demonstrated that cyclosporine A is an inhibitor of acetylcholinesterase activity and this effect is increased after an event of toxic demyelination of the central nervous system.
ESTHER : Mazzanti_2007_Int.J.Dev.Neurosci_25_259
PubMedSearch : Mazzanti_2007_Int.J.Dev.Neurosci_25_259
PubMedID: 17467222

Title : Acetylcholinesterase activity in rats experimentally demyelinated with ethidium bromide and treated with interferon beta - Mazzanti_2006_Neurochem.Res_31_1027
Author(s) : Mazzanti CM , Spanevello RM , Pereira LB , Goncalves JF , Kaizer R , Correa M , Ahmed M , Mazzanti A , Festugatto R , Graca DL , Morsch VM , Schetinger MR
Ref : Neurochem Res , 31 :1027 , 2006
Abstract : The ethidium bromide (EB) demyelinating model was associated with interferon beta (IFN-beta) to evaluate acetylcholinesterase (AChE) activity in the striatum (ST), hippocampus (HP), cerebral cortex (CC), cerebellum (CB), hypothalamus (HY), pons (PN) and synaptosomes from the CC. Rats were divided into four groups: I control (saline), II (IFN-beta), III (EB) and IV (EB and IFN-beta). After 7, 15 and 30 days rats (n = 6) were sacrificed, and the brain structures were removed for enzymatic assay. AChE activity was found to vary in all the brain structures in accordance with the day studied (7-15-30 days) (P < 0.05). In the group III, there was an inhibition of the AChE activity in the ST, CB, HY, HP and also in synaptosomes of the CC (P < 0.05). It was observed that IFN-beta per se was capable to significantly inhibit (P < 0.05) AChE activity in the ST, HP, HY and synaptosomes of the CC. Our results suggest that one of the mechanisms of action of IFN-beta is through the inhibition of AChE activity, and EB could be considered an inhibitor of AChE activity by interfering with cholinergic neurotransmission in the different brain regions.
ESTHER : Mazzanti_2006_Neurochem.Res_31_1027
PubMedSearch : Mazzanti_2006_Neurochem.Res_31_1027
PubMedID: 16871442

Title : Ethidium bromide inhibits rat brain acetylcholinesterase activity in vitro - Mazzanti_2006_Chem.Biol.Interact_162_121
Author(s) : Mazzanti CM , Spanevello RM , Obregon A , Pereira LB , Streher CA , Ahmed M , Mazzanti A , Graca DL , Morsch VM , Schetinger MR
Ref : Chemico-Biological Interactions , 162 :121 , 2006
Abstract : Ethidium bromide (EtBr), a fluorescent dark red compound and stain for double-stranded DNA and RNA was used to study acetylcholinesterase (AChE) activity in vitro together with kinetic parameters of this enzyme in the striatum (ST), hippocampus (HP), cerebral cortex (CC) and cerebellum (CB) of adult rats. AChE activity in vitro in the ST, HP, CC and CB was significantly reduced (p<0.05) in the presence of EtBr at concentrations of 0.00625, 0.0125, 0.025, 0.05 and 0.1 mM. For the analysis of the kinetic three concentrations of EtBr were tested (0.00625, 0.025 and 0.1 mM). An uncompetitive inhibition type was observed in the ST, HP and CC, whereas in the CB the inhibition type was mixed. These data indicate that EtBr should be considered a strong inhibitor of AChE activity demonstrating that there is an interaction between this compound and the cholinergic system.
ESTHER : Mazzanti_2006_Chem.Biol.Interact_162_121
PubMedSearch : Mazzanti_2006_Chem.Biol.Interact_162_121
PubMedID: 16839531