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Navegando por Orientadores "OLIVEIRA, Karen Renata Herculano Matos"

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    Avaliação dos níveis extracelulares de GABA e glutamato no sistema nervoso central de camundongos infectados com Plasmodium berghuei ANKA
    (Universidade Federal do Pará, 2024-11) LIMA, Renato Mateus Santos de; OLIVEIRA, Karen Renata Herculano Matos; http://lattes.cnpq.br/3032008039259369
    Cerebral malaria (CM) caused by Plasmodium falciparum results in high mortality, especially in children under 5, with up to 25% of survivors experiencing neurological sequelae such as cognitive impairment and seizures. The neurochemical mechanisms behind these impairments are not well understood. This study aimed to characterize changes in the levels of the neurotransmitters glutamate (GLU) and γ-Aminobutyric acid (GABA) in the central nervous system (CNS) during experimental cerebral malaria (ECM). ECM was induced in Swiss mice with Plasmodium berghei ANKA (PbA), and the animals were monitored for parasitemia, survival, and neurological impairments using the Rapid Murine Coma and Behavior Scale (RMCBS). On the 7th day post-infection (d.p.i), blood-brain barrier (BBB) disruption was assessed using Evans Blue dye, and glial cell evaluation was performed by immunofluorescence. Results showed that PbA-infected mice began to succumb to CM by the 6th d.p.i, with 100% mortality by the 10th d.p.i. Behavioral impairments were observed from the early stages of infection. Significant BBB permeability changes and increased expression of glial activation markers were noted in infected mice. There was a marked increase in GLU levels in the brain and cerebellum on days 3, 5, and 7 post-infection. GABA levels increased on days 3 and 5, returning to control levels by day 7. These findings indicate significant neurochemical alterations in GABAergic and glutamatergic neurotransmission, accompanied by neurological and vascular impairments, suggesting their involvement in the development of neurological symptoms in CM.
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    Caracterização da resposta inflamatória e alterações neuroquímicas e eletrofisiológicas do tecido retiniano em modelo murino de malária cerebral induzido pela infecção por Plasmodium Berghei ANKA
    (Universidade Federal do Pará, 2015-02-19) LEÃO, Luana Ketlen Reis; SILVA, Anderson Manoel Herculano Oliveira da; http://lattes.cnpq.br/8407177208423247; OLIVEIRA, Karen Renata Herculano Matos; http://lattes.cnpq.br/3032008039259369
    Cerebral malaria (CM) is one of the most serious complications resulting from infection by P. falciparum and the leading cause of death in children. The CM frame has a complex pathogenesis associated with neurological complications arising in an enhanced immune response as well as hemorrhagic events. Studies describing retinopathy associated with the frame, together with an intense process of astrogliosis in the vicinity of retinal vessels that nourish the tissue. This paper sought to characterize the inflammatory process and the possible neurochemical and electrophysiological changes in the retinal tissue of Swiss albino mice, when inoculated with Plasmodium berghei ANKA strain (PbA). Swiss albino mice were infected with PbA strain. To characterize the above experimental cerebral malaria (ECM) was evaluated several parameters, such as onset of clinical signs, survival curves parasitemia (%) and body mass gain, vascular permeability and quantification of cytokines (TNF-α, IL-6 and IL-10) in the cortical tissue. To evaluate changes in retinal tissue functionality, use full-field electroretinography. For the evaluation of neurotransmitter systems release assay was performed and uptake of glutamate and GABA which was then quantified by High Performance Liquid Chromatography. The inflammatory response analysis was performed to quantify the cytokines (TNF-α, IL-6 and IL-10) in retinal tissue. After characterizing the MCE framework we observe a reduction in the amplitude of b-wave of rods and cones, as well as increase the implicit time of rods, mixed responses at different intensities and oscillatory potential. We observed an increase in the release and glutamate uptake and also the activation of an anti-inflammatory pathway in retinal tissue. This study allowed us to validate the murine model of MCE and characterize for the first time, changes in the retinal function accompanied by changes in the glutamatergic system as well as activation of the inflammatory pathway in retinal tissue.
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    A infecção por Plasmodium berghei (ANKA) induz um quadro de encefalopatia hepática em modelo murino de malária não complicada
    (Universidade Federal do Pará, 2024-02) KAUFFMANN, Nayara; SILVA, Anderson Manoel Herculano Oliveira da; http://lattes.cnpq.br/8407177208423247; https://orcid.org/0000-0003-4022-8096; OLIVEIRA, Karen Renata Herculano Matos; http://lattes.cnpq.br/3032008039259369
    Introduction. The main changes in hepatocellular dysfunction associated with malaria are liver failure, hepatosplenomegaly and increased liver enzymes. Several studies have already elucidated that such liver changes can be caused by increased ammonia levels, which can consequently lead to dysfunction in the central nervous system (CNS), causing hepatic encephalopathy, culminating in an increase in the inflammatory response, cerebral edema, deregulation of neurotransmitters and cognitive and locomotor changes. Objective: To characterize possible changes in the central nervous system resulting from liver injury induced by Plasmodium berghei ANKA infection in a murine model of uncomplicated malaria. Methodology. For this, mice of the Balb-c lineage (20- 25g) were used between 45-54 postnatal days (CEUA nº 2229290317), inoculated with ~106 parasitized erythrocytes intraperitoneally. The experimental design was divided into two parts: Firstly, the survival curve, parasitemia, body mass, clinical signs, hepatic and histological changes, neurochemistry, presence of cerebral edema, vascular extravasation, inflammatory response, behavioral changes and quantification of blood levels were characterized. ammonia in the control and PbA groups. Subsequently, a treatment with lactulose was carried out to verify whether the changes found in the previous experiments were due to the increase in ammonia levels in the animals' brains. For this purpose, the groups were divided into: control group, lactulose 3mg/kg, PbA and PbA+lactulose 3mg/kg, in which the survival curve, parasitemia and locomotor activity were evaluated using the SHIRPA protocol. The results were expressed as mean+standard deviation. ANOVA (one way) was performed, post Tukey test, considering p<0.05 as significant. Results. Our data demonstrated that the PbA group presented changes in liver functions such as increased levels of AST and ALP, BT and BD, morphological changes such as hepatosplenomegaly, in addition to histological changes showing inflammatory infiltrate, deposition of malarial pigment and Kupffer cell hyperplasia, thus demonstrating a picture of liver failure. After characterizing the liver injury, we sought to understand whether these changes could generate impairment in the CNS, which we observed cognitive and motor impairment, in addition to changes in the levels of the neurotransmitters GABA and glutamate, accompanied by an increase in the inflammatory response, cerebral edema and dysfunction in the liver. blood-brain barrier. Once liver failure was demonstrated and, consequently, the presence of cognitive and behavioral changes, we sought to evaluate ammonia levels in the brains of control and PbA animals in the initial phase of infection. In this sense, the quantification of ammonia levels showed an increase on the 10th d.p.i., in brain tissue when compared to the control group, in which the levels were within expectations in relation to locomotor activity, when applying the protocol in the infected and treated group with lactulose, it was possible to observe that the PbA group showed changes in motor behavior, when compared to the control group. In contrast, the PbA+Lactulose 3mg/kg group showed an attenuation of cognitive and behavioral changes, showing that therapy with lactulose can attenuate the cognitive condition regarding motor behavior, muscle strength and tone, reflexes, and sensory function. Conclusion. We conclude that liver failure causes hepatic encephalopathy in a murine model of uncomplicated malaria, which culminates in changes in the central nervous system, by increasing ammonia levels in the brain, and by sequestering ammonia with the help of treatment. with lactulose at a dose of 3mg/kg, it can attenuate the neurological damage of animals with uncomplicated malaria, demonstrating that the behavioral changes come from a condition of hepatic encephalopathy, caused by increased levels of ammonia in the cortex of infected animals.
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    Melatonina previne danos cerebrais e déficits cognitivos induzidos pela infecção por Plasmodium berghei anka em modelo murino de malária cerebral
    (Universidade Federal do Pará, 2021-05) ATAIDE, Brenda Jaqueline de Azevedo; OLIVEIRA, Karen Renata Herculano Matos; http://lattes.cnpq.br/3032008039259369
    Cerebral malaria is characterized by permanent cognitive impairments in Plasmodium-infected children. Antimalarial therapies show little effectiveness to avoid neurological deficits and nervous tissue alterations elicited by severe malaria. Melatonin is a well-recognized endogenous hormone involved in the control of brain functions and maintenance of blood–brain barrier integrity. The current study has evaluated the effect of melatonin on the histological alterations, blood–brain barrier leakage, and neurocognitive impairments in mice developing cerebral malaria. Swiss mice infected with Plasmodium berghei ANKA strain was used as cerebral malaria model. Melatonin treatment (5 and 10 mg/kg) was performed for four consecutive days after the infection, and data have shown an increased survival rate in infected mice treated with melatonin. It was also observed that melatonin treatment blocked brain edema and prevented the breakdown of blood–brain barrier induced by the Plasmodium infection. Furthermore, hematoxylin and eosin staining revealed that melatonin mitigates the histological alterations in Plasmodium-infected animals. Melatonin was also able to prevent motor and cognitive impairments in infected mice. Taken together, these results show for the first time that melatonin treatment prevents histological brain damages and neurocognitive alterations induced by cerebral malaria
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    Receptor A2A de adenosina modula o transporte de glutamato independente de sodio em cultura primaria de celulas da retina
    (Universidade Federal do Pará, 2024-11) LIMA, Caroline Araujo Costa de; OLIVEIRA, Karen Renata Herculano Matos; http://lattes.cnpq.br/3032008039259369
    Dysregulation of extracellular glutamate levels is directly associated with several CNS pathologies, highlighting the importance of glutamate transporters in maintaining tissue homeostasis and developing new therapeutic approaches. The retina is particularly vulnerable toexcitotoxic events due to its high levels of glutamate extracelular and the frequente exposure to oxidative stimuli, reinforcing the need for regulatory mecanisms to preserve retinal physiology. In this context, adenosine emerges as an essential neuromodulator, exhibiting regulatory effects that are concentration- and receptor-dependent. Therefore, the objetive of this study was to characterize the effect of adenosine on sodium-independent glutamate transport in retinal cell culture. As such, mixed primary cell cultures from White leghorn chick embryos (E7-E8) were maintained for 7 days in DMEM+10% FBS at 37°C and 5% CO₂. The cells were submitted to apre-incubation with an A2A receptor blocker and incubated with different adenosine concentrations for glutamate release and uptake assays. Glutamate levels were quantified by HPLC, and protein levels were measured by the Bradford method, with equimolar substitution of NaCl by LiCl. Furthermore, immunofluorescence with an anti-xCT antibody and the nuclear marker DAPI was used to identify the sodium-independent glutamate transporter, with image analysis performed using ImageJ e Photoshop CS6. Statistical analysis was conducted using Student’s test T and ANOVA one-way with Tukey post-hoc test via GraphPad 9.0, with data expressed as percentage of control±S.D. with p<0,05. The results confirmed the expression of the xCT subunit, indicating that the system xCG-is the sodium-independent glutamate transporter in retinal cells. Additionally, adenosine at a concentration of 50μM increased glutamate release by approximately 800%, while glutamate sodium-independent uptake was completely inhibited.These effects were fully by A2A receptor blockade. Therefore, we demonstrated that activation of the A2A receptor modulates glutamate sodium independent transport, whose
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    O transportador XCG- medeia a captação de glutamato independente de sódio em cultura primária de células gliais da cóclea de camundongos neonatos
    (Universidade Federal do Pará, 2022-10-20) MARTINS, Luana Carvalho; OLIVEIRA, Karen Renata Herculano Matos; http://lattes.cnpq.br/3032008039259369
    The cochlea is a sensory organ of the auditory system whose excitatory synapses are mediated by L-Glutamate. Since glutamate has physiological and pathological repercussions on the cochlea, the crucial role of glutamate transport mechanisms capable of regulating the extracellular concentration of this neurotransmitter in order to maintain auditory function is highlighted. Within this context, in this study we sought to investigate the activity and expression of glutamate transport systems in an in vitro model of primary cultures of cochlear glial cells obtained from newborn mice of the Balb/C lineage. For this, we determined the sodium dependent and independent glutamate transport by means of glutamate uptake and release assays whose extracellular concentrations were quantified using High Performance Liquid Chromatography coupled to a fluorescence detector. Finally, the cells were subjected to immunofluorescence assay for XCG sodium-independent glutamate transporter labeling. In our results, we demonstrate that cochlear glial cells have a glutamate transport system mediated by the XCG- transporter. Such data suggest a possible role of this transporter in the control of extracellular concentrations of glutamate and regulation of the redox state, which may help to preserve auditory function.
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    O tratamento com glutationa potencializa o dano hepático em camundongos infectados com Plasmodium berghei (ANKA)
    (Universidade Federal do Pará, 2016-05-10) KAUFFMANN, Nayara; OLIVEIRA, Karen Renata Herculano Matos; http://lattes.cnpq.br/3032008039259369
    Malaria is a disease caused by protozoa of the genus Plasmodium and presents itself as a major public health problems in the world. To evaluate the malaria frame, murine models have been used for its similarities between species infective for mice and species infective to man. The increased production of reactive oxygen species and changes in the activity of enzymes such as glutathione peroxidase and superoxide dismutase have been characterized within the clinical picture of the disease, but little is known about the participation of antioxidant molecules such as glutathione in the evolution of the disease. Given the above, the main objective of this study is to evaluate the effect of glutathione in the evolution of murine malaria frame and front to damage caused by infection with Plasmodium berghei ANKA strain (PbA). To this were Balb-C mice, which were inoculated (~106 parasitized erythrocytes) intraperitoneally. The groups were divided into malaria group (PbA), PbA group + GSH 1 mg, PbA group + GSH 3 mg and PbA group + GSH 8 mg treated for 7 days consecutive. The development of the disease was monitored daily by determining the survival, body mass and parasitaemia was monitored every three days in blood strains, was also analyzed the histological sections of liver tissue was performed and the biochemical analysis of liver transaminases. Our data demonstrated that treatment with GSH (8mg/kg) accelerated mortality of infected animals once between days 13-14 after infection about 43% of the animals progressed to death. In the group infected with PbA that received no treatment with GSH, a similar reduction (40%) was observed only from 23-25 days post infection. In relation to PbA + GSH 1mg groups and GSH + PbA 3 mg, there was no difference when compared to the PbA group. Interestingly, although treatment with GSH 8mg has accelerated mortality in the infected group, no significant difference in parasitaemia level of the four groups analyzed. In relation to body mass was observed a difference between day 0 and 24 in all groups, but when analyzed between groups. In what concerns the histological and biochemical tests, we noted that listen both changes in histology and in transaminase, with the latter being expressed in PbA changes group was treated with glutathione 8mg / kg group than in PbA. Concluding that glutathione when administered intraperitoneally accelerates the mortality of mice infected with the ANKA strain, but this mortality is not associated with increased parasitemia, then indicating that mortality may result from liver changes.
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