Browsing by Author "Figueiredo, Vivian Paulino"

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    Antioxidant effects of oral Ang-(1-7) restore insulin pathway and RAS components ameliorating cardiometabolic disturbances in rats.
    (2019) Figueiredo, Vivian Paulino; Barbosa, Maria Andréa; Castro, Uberdan Guilherme Mendes de; Zacarias, Aline Cruz; Bezerra, Frank Silva; Cota, Renata Guerra de Sá; Lima, Wanderson Geraldo de; Santos, Robson Augusto Souza dos; Alzamora, Andréia Carvalho
    In prevention studies of metabolic syndrome (MetS), Ang-(1-7) has shown to improve the insulin signaling. We evaluated the HPβCD/Ang-(1-7) treatment on lipid metabolism, renin-angiotensin system (RAS) components, oxidative stress, and insulin pathway in the liver and gastrocnemius muscle and hepatic steatosis in rats with established MetS. After 7 weeks of high-fat (FAT) or control (CT) diets, rats were treated with cyclodextrin (HPβCD) or HPβCD/Ang-(1-7) in the last 6 weeks. FATHPβCD/ empty rats showed increased adiposity index and body mass, gene expression of ACE/ANG II/AT1R axis, and oxidative stress. These results were accompanied by imbalances in the insulin pathway, worsening of liver function, hyperglycemia, and dyslipidemia. Oral HPβCD/Ang-(1-7) treatment decreased ACE and AT1R, increased ACE2 gene expression. in the liver, and restored thiobarbituric acid reactive substances (TBARS), catalase (CAT), superoxide dismutase (SOD), insulin receptor substrate (Irs-1), glucose transporter type 4 (GLUT4), and serine/threonine kinase 2 (AKT-2) gene expression in the liver and gastrocnemius muscle improving hepatic function, cholesterol levels, and hyperglycemia in MetS rats. Overall, HPβCD/Ang-(1-7) treatment restored the RAS components, oxidative stress, and insulin signaling in the liver and gastrocnemius muscle contributing to the establishment of blood glucose and lipid homeostasis in MetS rats.
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    Avaliação de parâmetros inflamatórios na infecção aguda e crônica de camundongos infectados pelo Trypanosoma cruzi e submetidos à dieta hiperlipídica.
    (2016) Figueiredo, Vivian Paulino; Silva, André Talvani Pedrosa da; Silva, André Talvani Pedrosa da; Costa, Daniela Caldeira; Pedrosa, Maria Lúcia; Veloso, Vanja Maria
    O estado nutricional vem se destacando nas interações entre agentes infecciosos e a resposta imunofisiológica de seus hospedeiros apresentando-se diretamente ligado à qualidade da dieta na qual o indivíduo é submetido. Como exemplo, uma dieta rica em lipídeos pode desencadear alterações metabólicas e cardiovasculares. Na linha das alterações cardiovasculares, a infecção pelo protozoário Trypanosoma cruzi aparece como uma condição predisponente, ao lado da resposta imune do hospedeiro infectado. Assim, este estudo objetiva avaliar a interferência da dieta hiperlipídica (DH) no processo inflamatório agudo e crônico da infecção experimental pelo T. cruzi. Para tanto, foram utilizados camundongos machos da linhagem C57BL/6 divididos em 4 grupos: (i) dieta convencional, (ii) dieta convencional infectado com a cepa VL-10 do T. cruzi, (iii) DH e (iv) DH infectado com o T. cruzi. Os animais foram eutanasiados ao final de 12 semanas de dieta e após um mês de infecção (fase aguda) e ao final de 22 semanas de dieta e 100 dias de infecção (fase crônica). Os resultados indicam que a DH foi capaz de elevar a massa corporal, a quantidade de tecido adiposo nos animais, a parasitemia e os níveis circulantes de colesterol total e HDL. Relativo ao contexto inflamatório, houve elevação de IL-10 e TNF plasmática nos animais infectados, independentemente da dieta, em contrapartida aos valores reduzidos de leptina. O infiltrado inflamatório cardíaco também apresentou-se elevado nos animais submetidos à DH em concordância com a elevação nos lipídeos totais e presença de esteatose hepática, sendo a maior inflamação associada à infecção. Ao contrário da MMP9, a atividade da MMP2 mostrou-se elevada no tecido cardíaco dos animais infectados e submetidos à DH na fase aguda. Nossos dados sugerem que a DH interfere na imunopatogênese tanto cardíaca quanto hepática e eleva a atividade de MMP2 e o remodelamento cardíaco em animais infectados pelo T. cruzi.
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    Benznidazole microcrystal preparation by solvent change precipitation and in vivo evaluation in the treatment of Chagas disease.
    (2011) Maximiano, Flávia Pires; Paula, Lívia Maria de; Figueiredo, Vivian Paulino; Andrade, Isabel Mayer de; Silva, André Talvani Pedrosa da; Barreto, Lívia Cristina Lira de Sá; Bahia, Maria Terezinha; Cunha Filho, Marcílio Sérgio Soares da
    Benznidazole (BNZ) is traditionally used to treat Chagas disease. Despite its common use, BNZ has a poor water solubility and a variable bioavailability. The purpose of this study was to prepare BNZ microcrystals by solvent change precipitation and to study the effects of BNZ micronisation on therapeutic efficiency using a murine model of Chagas disease. The solvent change precipitation procedure was optimised in order to obtain stable and homogeneous particles with a small particle size, high yield and fast dissolution rate. The thermal and crystallographic analysis showed no polymorphic change in the microcrystals, and microscopy confirmed a significant reduction in particle size. A marked improvement in the drug dissolution rate was observed for micronised BNZ particles and BNZ tablets in comparison with untreated BNZ and commercial Rochagan_. In vivo studies showed a significant increase in the therapeutic efficacy of the BNZ microparticles, corroborating the dissolution results.
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    Caracterização dos aspectos inflamatório e funcionais do ventrículo esquerdo em cães infectados com a cepa Berenice 78 do Trypanosoma cruzi após terapia com doxiciclina e benznidazol.
    (2018) Lopes, Laís Roquete; Silva, André Talvani Pedrosa da; Figueiredo, Vivian Paulino; Silva, André Talvani Pedrosa da; Silva, Glenda Nicioli da; Estanislau, Juliana de Assis Silva Gomes; Silva, Marcelo Eustáquio; Giunchetti, Rodolfo Cordeiro
    A cardiopatia chagásica (CC) induzida pelo Trypanosoma cruzi é uma manifestação clínica dependente da resposta inflamatória gerada pelo hospedeiro, ocasionando destruição celular/tecidual e, consequente, remodelamento na matriz extracelular cardíaca. Citocinas, quimiocinas e outras proteínas solúveis ou de membrana participam desta resposta imune e, por isso, estratégias farmacológicas para regular estes mediadores e desacelerar o remodelamento cardíaco na CC tornam-se importantes focos de investigação. Na presente proposta, 30 cães sem raça definida foram infectados (ou não) pela cepa Berenice-78 (Be-78) do T. cruzi e submetidos ao tratamento diário com doses sub-antimicrobial do antibiótico doxiciclina/Dox durante 12 meses de infecção (sendo 50mg/Kg manhã e 50mg/kg noite), em associação (ou não) com o tratamento por 60 dias com o Benznidazol/Bz (7mg/kg – administrado à partir do 8º mês de infecção), fármaco com ação anti-T. cruzi. Antes e durante os 12 meses de infecção, estes animais foram avaliados trimestralmente quanto à função cardíaca (ecocardiografia/ECO) e, após a eutanásia, o tecido cardíaco (átrios e ventrículos) dos animais foram conservados para avaliação: (i) dos aspectos histopatológicos (ii) da cinética da CCL2 plasmática e ventricular esquerda e da expressão dos receptores de quimiocinas (CCR3 a 6, CCR8 e CXCR3), ambos no ventrículo esquerdo (VE). Estes parâmetros foram avaliados, em paralelo à análise ecocardiográfica. Observamos que os tratamentos reduziram a massa cardíaca nos animais. A avaliação histológica mostrou aumento do infiltrado inflamatório no VE dos animais infectados, mas Dox conseguiu reduzi-lo. A produção de CCL2, TNF e IFN-gama no VE foi semelhante em todos os animais infectados, mas no plasma aumentaram no 14º mês de tratamento em relação ao grupo não infectado. Juntos, esses dados apontam para o potencial papel das doses sub-antimicrobianas de Dox, em associação com o Bz, como estratégia farmacológica de melhora morfofuncional cardíaca associada à infecção pelo T. cruzi. Entretanto, novos estudos com diferentes populações genéticas do parasita e com o estudo da farmacocinética de Dox merecem atenção para consolidar essa proposta.
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    CXCL-16, IL-17, and bone morphogenetic protein 2 (BMP-2) are associated with overweight and obesity conditions in middle-aged and elderly women.
    (2017) Ribeiro, Silvana Mara Luz Turbino; Lopes, Laís Roquete; Costa, Guilherme de Paula; Figueiredo, Vivian Paulino; Bajracharya, Deena Shrestha; Batista, Aline Priscila; Nicolato, Roney Luiz de Carvalho; Oliveira, Fernando Luiz Pereira de; Estanislau, Juliana de Assis Silva Gomes; Silva, André Talvani Pedrosa da
    The current concept of overweight/obesity is most likely related to a combination of increased caloric intake and decreased energy expenditure. Widespread inflammation, associated with both conditions, appears to contribute to the development of some obesity-related comorbidities. Interventions that directly or indirectly target individuals at high risk of developing obesity have been largely proposed because of the increasing number of overweight/obese cases worldwide. The aim of the present study was to assess CXCL16, IL-17, and BMP-2 plasma factors in middle-aged and elderly women and relate them to an overweight or obese status. In total, 117 women were selected and grouped as eutrophic, overweight, and obese, according to anthropometric parameters. Analyses of anthropometric and circulating biochemical parameters were followed by plasma immunoassays for CXCL-16, IL- 17, and BMP-2.
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    High fat diet modulates inflammatory parameters in the heart and liver during acute Trypanosoma cruzi infection.
    (2018) Figueiredo, Vivian Paulino; Lopes Júnior, Evandro Saraiva; Lopes, Laís Roquete; Simões, Natalia Figuerôa; Penitente, Arlete Rita; Bearzoti, Eduardo; Vieira, Paula Melo de Abreu; Schulz, Richard; Silva, André Talvani Pedrosa da
    The high fat diet (HFD) can trigger metabolic and cardiovascular diseases. Trypanosoma cruzi infection induces progressive inflammatory manifestations capable to affect the structure and the function of important organs such as the heart and liver. Here we aimed to investigate the effects of a HFD on the immune response and matrix metalloproteinase (MMP) activities during acute infection with the T. cruzi strain VL-10. The VL-10 strain has cardiac tropism and causes myocarditis in mice. Male C57BL/6 mice were treated with either: (i) regular diet (Reg) or (ii) HFD for 8 weeks, after which mice in each group were infected with T. cruzi. Mice were euthanized on day 30 after infection, and the liver and heart were subjected to histology and zymography to determine MMP-2 activities and plasma levels of IL-10, TNF, CCL2, and CCL5. T. cruzi-infected HFD animals had higher parasitemia, LDL and total cholesterol levels. Regardless of diet, plasma levels of all inflammatory mediators and cardiac MMP-2 activity were elevated in infected mice in contrast with the low plasma levels of leptin. HFD animals presented micro- and macrovesicular hepatic steatosis, while cardiac leukocyte infiltration was mainly detected in T. cruzi-infected mice. Our findings suggested that a HFD promotes higher circulating T. cruzi load and cardiac and liver immunopathogenesis in an experimental model using the VL-10 strain of the T. cruzi.
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    A high-fat diet exacerbates the course of experimental Trypanosoma cruzi infection that can be mitigated by treatment with Simvastatin.
    (2020) Souza, Débora Maria Soares de; Costa, Guilherme de Paula; Leite, Ana Luísa Junqueira; Oliveira, Daniela Silva de; Pinto, Kelerson Mauro de Castro; Farias, Sílvia Elvira Barros; Simões, Natália Figueira; Paiva, Nívia Carolina Nogueira de; Vieira, Paula Melo de Abreu; Silva, Camilo Adalton Mariano da; Figueiredo, Vivian Paulino; Menezes, Ana Paula de Jesus; Silva, André Talvani Pedrosa da
    The protozoan Trypanosoma cruzi is responsible for triggering a damage immune response in the host cardiovascular system. This parasite has a high affinity for host lipoproteins and uses the low-density lipoprotein (LDL) receptor for its invasion. Assuming that the presence of LDL cholesterol in tissues could facilitate T. cruzi proliferation, dietary composition may affect the parasite-host relationship. Therefore, the aim of this study was to evaluate myocarditis in T. cruzi-infected C57BL/6 mice—acute phase—fed a high-fat diet and treated with simvastatin, a lipid-lowering medication. Animals (n = 10) were infected with 5 × 103 cells of the VL-10 strain of T. cruzi and treated or untreated daily with 20 mg/kg simvastatin, starting 24 h after infection and fed with a normolipidic or high-fat diet. Also, uninfected mice, treated or not with simvastatin and fed with normolipidic or high-fat diet, were evaluated as control groups. Analyses to measure the production of chemokine (C-C motif) ligand 2 (CCL2), interferon- (IFN-) γ, interleukin- (IL-) 10, and tumor necrosis factor (TNF); total hepatic lipid dosage; cholesterol; and fractions, as well as histopathological analysis, were performed on day 30 using cardiac and fat tissues. Our results showed that the high-fat diet increased (i) parasite replication, (ii) fat accumulation in the liver, (iii) total cholesterol and LDL levels, and (iv) the host inflammatory state through the production of the cytokine TNF. However, simvastatin only reduced the production of CCL2 but not that of other inflammatory mediators or biochemical parameters. Together, our data suggest that the high-fat diet may have worsened the biochemical parameters of the uninfected and T. cruzi-infected animals, as well as favored the survival of circulating parasites.
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    A infecção experimental pelo Trypanosoma cruzi agrava o desenvolvimento de lesões ateroscleróticas em camundongos apoE-/-.
    (Programa de Pós-Graduação em Ciências Biológicas. Núcleo de Pesquisas em Ciências Biológicas, Pró-Reitoria de Pesquisa e Pós Graduação, Universidade Federal de Ouro Preto., 2012) Figueiredo, Vivian Paulino; Silva, André Talvani Pedrosa da
    A resposta inflamatória sistêmica desencadeada por alguns agentes infecciosos exercem efeitos pró-aterogênicos via produção e ação de mediadores inflamatórios sobre a parede vascular. Nesse contexto, a infecção desencadeada pelo protozoário Trypanosoma cruzi apresenta um caráter inflamatório responsável pelo desenvolvimento de inúmeras manifestações cardiovasculares enquanto a aterosclerose, doença crônico-degenerativa, também é capaz de ocasionar obstrução de artérias pelo acúmulo de lipídeos em suas paredes através de um evento inflamatório local. A saber, a apolipoproteína E (apoE) é a principal glicoproteína responsável pelo transporte e metabolismo de colesterol e triglicerideos, sendo uma constituinte das lipoproteínas VLDL, HDL e quilomícrons. Neste estudo avaliamos a interferência da apoE no desenvolvimento das lesões cardiovasculares em camundongos C57BL/6 (n=28) e apoE knockout/ -/- (n=28) com 10 semanas, infectados pelas cepas Berenice 78 (Be 78) e Colombiana do T. cruzi. Avaliou-se diariamente a parasitemia e semanalmente o peso dos animais. Antes e após 30 dias de infecção, coletou-se sangue para dosagens bioquímicas (colesterol total, colesterol HDL e triglicérideos) e imunológicas (CCL2/MCP-1 e CCL5/RANTES). Após a eutanásia, o fígado e as fezes foram utilizados para extração e quantificação dos lipídeos totais e o arco aórtico, juntamente com o tecido muscular cardíaco, para avaliações morfométricas. Observou-se um menor período pré-patente nos animais selvagens (dia 9) em relação aos apoE-/- (dia 12), sendo que nestes últimos a parasitemia foi menor para ambas as cepas estudadas. Não houve diferença no peso dos animais entre os grupos, mas o colesterol total e os triglicerídeos plasmáticos mostraram-se elevados no grupo apoE-/-. Em relação à genética do parasito, a cepa Be 78 nos animais apoE-/- mostrou-se associada ao aumento dos lipídeos fecais, enquanto a cepa Colombiana neste mesmo grupo apresentou-se associada a níveis elevados de triglicérideos plasmáticos. Na análise plasmática de quimiocinas, verificou-se elevada produção de CCL2 e CCL5 em todos os animais infectados, porém apenas com a cepa Be 78, avaliada em animais apoE-/-, houve uma redução dos níveis séricos de CCL5. Observou-se aumento de células inflamatórias no tecido cardíaco, bem como de parasitos teciduais, no grupo infectado com a cepa Colombiana. Em relação à aterogênese, o grupo apoE-/- infectado por esta cepa, apresentou maiores áreas de lesão e alterações no conteúdo de colágeno. Estes dados sugerem que a infecção experimental pelo T. cruzi interfere no desenvolvimento de lesões ateroscleróticas em camundongos apoE-/-, assim como na produção de mediadores inflamatórios plasmáticos e de alguns tipos lipídicos. A análise e compreensão da interferência da apoE na patogênese cardíaca da doença de Chagas associado à variabilidade genética do parasito constituirão importantes elementos para estudos futuros envolvendo a resposta inflamatória cardiovascular.
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    Low doses of Simvastatin therapy ameliorate cardiac inflammatory remodeling in Trypanosoma cruzi-Infected dogs.
    (2011) Melo, Lilian; Caldas, Ivo Santana; Azevedo, Maíra Araújo; Gonçalves, Karolina Ribeiro; Nascimento, Alvaro Fernando da Silva do; Figueiredo, Vivian Paulino; Diniz, Lívia de Figueiredo; Lima, Wanderson Geraldo de; Torres, Rosália Morais; Bahia, Maria Terezinha; Silva, André Talvani Pedrosa da
    Chagas cardiomyopathy remodeling is based on the presence of Trypanosoma cruzi in heart tissue and on the complex inflammatory response leading to a myocardium fibrosis and alterations in conductive and functional heart parameters. This study aims to evaluate Simvastatin on the inflammatory response and heart functionality using dogs infected with Y strain of T. cruzi . Animals were treated daily with Simvastatin (20 mg) for 6 months and submitted to clinical and immunopathological evaluations. Simvastatin reduced heart expression and serum levels of interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) but not interleukin-10 (IL-10), possibly favoring blood parasitism but reducing inflammation and fibrosis in the left ventricle and right atrium. Simvastatin also ameliorated ejection fraction, diastolic diameter, and mass index of the left ventricle 6 months after infection. This study suggests that more investigation should be performed on the use of statins as a prophylactic therapy against cardiac remodeling because of their effects on modifying immune response and benefiting functional parameters in dogs with T. cruzi -induced ventricular dysfunctions.
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    Lycopene pretreatment improves hepatotoxicity induced by acetaminophen in C57BL/6 mice.
    (2017) Bandeira, Ana Carla Balthar; Silva, Rafaella Cecília da; Rossoni Júnior, Joamyr Victor; Figueiredo, Vivian Paulino; Silva, André Talvani Pedrosa da; Cangussú, Silvia Dantas; Bezerra, Frank Silva; Costa, Daniela Caldeira
    Acetaminophen (APAP) is an antipyretic and analgesic drug that, in high doses, leads to severe liver injury and potentially death. Oxidative stress is an important event in APAP overdose. Researchers are looking for natural antioxidants with the potential to mitigate the harmful effects of reactive oxygen species in different models. Lycopene has been widely studied for its antioxidant properties. The aim of this study was to evaluate the antioxidant potential of lycopene pretreatment in APAP-induced liver injury in C57BL/6 mice. C57BL/6 male mice were divided into the following groups: control (C); sunflower oil (CO); acetaminophen 500 mg/kg (APAP); acetaminophen 500 mg/kg + lycopene 10 mg/kg (APAP + L10), and acetaminophen 500 mg/kg + lycopene 100 mg/kg (APAP + L100). Mice were pretreated with lycopene for 14 consecutive days prior to APAP overdose. Analyses of blood serum and livers were performed. Lycopene was able to improve redox imbalance, decrease thiobarbituric acid reactive species level, and increase CAT and GSH levels. In addition, it decreased the IL-1b expression and the activity of MMP-2. This study revealed that preventive lycopene consumption in C57BL/6 mice can attenuate the effects of APAP-induced liver injury. Furthermore, by improving the redox state, and thus indicating its potential antioxidant effect, lycopene was also shown to have an influence on inflammatory events.
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    Maternal high-fat diet triggers metabolic syndrome disorders that are transferred to first and second offspring generations.
    (2020) Barbosa, Claudiane Maria; Figueiredo, Vivian Paulino; Barbosa, Maria Andréa; Cardoso, Leonardo Máximo; Alzamora, Andréia Carvalho
    A high-fat (H) diet increases metabolic disorders in offspring. However, there is great variability in the literature regarding the time of exposure, composition of the H diets offered to the genitors and/or offspring and parameters evaluated. Here, we investigated the effect of a H diet subjected to the genitors on different cardio-metabolic parameters on first (F1)- and second (F2)-generation offspring. Female Fischer rats, during mating, gestation and breast-feeding, were subjected to the H diet (G0HF) or control (G0CF) diets. Part of F1 offspring becomes G1 genitors for generating the F2 offspring. After weaning, F1 and F2 rats consumed only the C diet. Nutritional, biometric, biochemical and haemodynamic parameters were evaluated. G0HF genitors had a reduction in food intake but energy intake was similar to the control group. Compared with the control group, the F1H and F2H offspring presented increased plasma leptin, insulin and fasting glucose levels, dietary intake, energy intake, adiposity index, mean arterial pressure, sympathetic drive evidenced by the hexamethonium and insulin resistance. Our data showed that only during mating, gestation and breast-feeding, maternal H diet induced cardio-metabolic disorders characteristic of human metabolic syndrome that were transferred to both females and males of F1 and F2 offspring, even if they were fed control diet after weaning. This process probably occurs due to the disturbance in mechanisms related to leptin that increases energy intake in F1H and F2H offspring. The present data reinforce the importance of balanced diet during pregnancy and breast-feeding for the health of the F1 and F2 offspring.
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    Oral Ang-(1-7) treatment improves white adipose tissue remodeling and hypertension in rats with metabolic syndrome.
    (2019) Barbosa, Maria Andréa; Sousa, Graziele Galdino de; Castro, Uberdan Guilherme Mendes de; Carneiro, Cláudia Martins; Figueiredo, Vivian Paulino; Cota, Renata Guerra de Sá; Santos, Robson Augusto Souza dos; Alzamora, Andréia Carvalho
    Objective: Angiotensin (Ang)-(1-7) has preventive effects on metabolic syndrome (MetS). The aim of this study was to evaluate the therapeutic effect of oral Ang-(1-7) on mean arterial pressure (MAP), insulin resistance (IR), inflammatory process, and remodeling of white adipose tissue (WAT) in rats with establishedMetS. Methods: Rats were subjected to control (CT; AIN-93M) or high-fat (HF) diets for 13 wk to induce MetS and treated with Ang-(1-7) or vehicle (V) for the last 6 wk. At the end of 13 wk, MAP, biochemical and histological parameters, and uncoupling protein (UCP) and inflammatory gene expression were determined by quantitative reverse transcription polymerase chain reaction. Results: HF-V rats showed increased visceral fat deposition, inflammatory cytokine expression, hyperplasia, and hypertrophy in retroperitoneal (WAT) and brown adipose tissue (BAT). Additionally, the gastrocnemius muscle reduced UCP-3 and increased the UCP-1 expression in BAT. HF-V also elevated levels of plasma insulin, glucose, homeostatic model assessment (HOMA) of IR and HOMA-b, and increased body mass, adiposity, and MAP. Ang-(1-7) treatment in rats with MetS [HF-Ang-(1-7)] reduced WAT area, number of adipocytes, and expression of proinflammatory adipokines in WAT and BAT and increased UCP-3 in gastrocnemius muscle and UCP-1 expression in BAT compared with the HF-V group. These events prevented body mass gain, reduced adiposity, and normalized fasting plasma glucose, insulin levels, HOMA-IR, HOMA-b, and MAP. Conclusion: Data from the present study demonstrated that oral Ang-(1-7) treatment is effective in restoring biochemical parameters and hypertension in established MetS by improving hypertrophy and hyperplasia in WAT and inflammation in adipose tissue, and regulating metabolic processes in the gastrocnemius muscle and BAT.
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    Potential role of Carvedilol in the cardiac immune response induced by experimental infection with Trypanosoma cruzi.
    (2017) Horta, Aline Luciano; Leite, Ana Luísa Junqueira; Costa, Guilherme de Paula; Figueiredo, Vivian Paulino; Silva, André Talvani Pedrosa da
    Trypanosoma cruzi causes a cardiac infection characterized by an inflammatory imbalance that could become the inciting factor of the illness. To this end, we evaluated the role of carvedilol, a beta-blocker with potential immunomodulatory properties, on the immune response in C57BL/6 mice infected with VL-10 strain of T. cruzi in the acute phase. Animals (𝑛 = 40) were grouped: (i) not infected, (ii) infected, (iii) infected + carvedilol, and (iv) not infected + carvedilol.We analyzed parameters related to parasitemia, plasma levels of TNF, IL-10, and CCL2, and cardiac histopathology after the administration of carvedilol for 30 days. We did not observe differences in the maximum peaks of parasitemia in the day of their detection among the groups. The plasma TNF was elevated at 60 days of infection in mice treated or not with carvedilol. However, we observed a decreased CCL2 level and increased IL-10 levels in those infected animals treated with carvedilol, which impacted the reduction of the inflammatory infiltration in cardiac tissue. For this experimentalmodel, carvedilol therapy was not able to alter the levels of circulating parasites butmodulates the pattern of CCL2 and IL-10 mediators when the VL10 strain of T. cruzi was used in C57BL6 mice.
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    Renovascular hypertension increases serum TNF and CX3CL1 in experimental Trypanosoma cruzi infection.
    (2018) Silva, M. C.; Azevedo, Maíra Araújo; Figueiredo, Vivian Paulino; Moura Junior, Manoel Ramos de; Coelho Júnior, Diógenes; Martinelli, Patrícia Massara; Machado, Raquel do Pilar; Alzamora, Andréia Carvalho; Silva, André Talvani Pedrosa da
    Trypanosoma cruzi triggers a progressive inflammatory response affecting cardiovascular functions in humans and experimental models. Angiotensin II, a key effector of the renin-angiotensin system, plays roles in mediating hypertension, heart failure, and inflammatory responses. T. cruzi and AngII can induce inflammatory responses by releasing inflammatory mediators. The aim of this study was to evaluate systemic AngII, tumor necrosis factor (TNF), and CX3CL1 mediators in a two-kidney one-clip (2K1C) renovascular hypertension model using Wistar rats infected with T. cruzi. Our data showed an increase in serum AngII in uninfected and T. cruzi-infected rats 1 week after 2K1C surgery compared to non-2K1C (Sham) animals. The baseline systolic blood pressure was higher in both uninfected and infected 2K1C rats. Despite no difference in circulating parasites in the acute phase of infection, elevated serum TNF and CX3CL1 were observed at 8 weeks post-infection in 2K1C rats in association with higher cardiac inflammatory infiltration. In summary, AngII-induced hypertension associated with T. cruzi infection may act synergistically to increase TNF and CX3CL1 in the 2K1C rat model, thereby intensifying cardiac inflammatory infiltration and worsening the underlying inflammation triggered by this protozoan.
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    The overweight increases circulating inflammatory mediators commonly associated with obesity in young individuals.
    (2018) Lopes, Laís Roquete; Ribeiro, Silvana Mara Luz Turbino; Figueiredo, Vivian Paulino; Leite, Ana Luísa Junqueira; Nicolato, Roney Luiz de Carvalho; Estanislau, Juliana de Assis Silva Gomes; Oliveira, Fernando Luiz Pereira de; Silva, André Talvani Pedrosa da
    Obesity is a serious and growing world healthy problem affecting developed and developing countries. The new conception of obesity as a basal inflammatory condition has opened a new window of possibilities to identify inflammatory biomarkers to be used in the diagnosis or prognosis of obesity-associated comorbidities. This present work aims the identification of the adipokines (leptin and resistin), chemokines (CCL2, CCL5, CXCL16) and the BMP-2 and their association with the clinical, biochemical (fasting glucose, hemogram, cholesterol, T3, T4 and TSH) and anthropometric (weight, height, body circumferences, skinfold thickness and percentage of body fat) parameters in young adults (18–30 years old) presenting obesity and overweight. Our data showed increasing in anthropometric parameters and in the plasma inflammatory levels in those individuals presenting overweight and obesity. We observed a higher plasma levels of CCL2, CCL5, CXCL16, leptin and resistin in those overweigh and obese individuals. In addition, the CCL2, CCL5 presented a positive correlation with the body mass index and the body fat percentage. Assuming the obesity as a systemic inflammatory process, in this current study, the overweight individuals possess a close similar pattern of circulating inflammatory mediators which might be a potential risk of the development of obesity comorbidities. Further studies are still needed to precise the role of the biomarkers CCL2, CCL5, CXCL16 and BMP-2 in the clinical prognosis related to the overweight or obese individuals.
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    The β-blocker carvedilol and the benznidazole modulate the cardiac immune response in the acute infection induced by Colombian strain of the Trypanosoma cruzi.
    (2018) Horta, Aline Luciano; Figueiredo, Vivian Paulino; Leite, Ana Luísa Junqueira; Costa, Guilherme de Paula; Menezes, Ana Paula de Jesus; Ramos, Camila de Oliveira; Pedrosa, Tamiles Caroline Fernandes; Bezerra, Frank Silva; Vieira, Paula Melo de Abreu; Silva, André Talvani Pedrosa da
    BACKGROUND The infection led by Trypanosoma cruzi persists in mammalian tissues causing an inflammatory imbalance. Carvedilol (Cv), a non-selective beta blocker drug indicated to treat heart failure and antihypertensive has shown to promote antioxidant and immunomodulatory properties which might improve the inflammation induced by T. cruzi. OBJECTIVES Evaluate the role of Cv on the inflammatory response of C57BL/6 mice acutely infected with the Colombian strain of T. cruzi. METHODS Animals were infected with the Colombian strain of T. cruzi and treated with Cv (25 mg/kg/day), benznidazole (Bz) (100 mg/kg/day) or their combination. On the 28th day of infection and 23 days of treatment, the euthanasia occurred, and the heart preserved for histopathological, oxidative stress (SOD, catalase, TBARs, carbonylated proteins) and plasma (CCL2, CCL5, TNF, IL-10) analyses. Parasitaemia and survival were assessed along the infection. FINDINGS Cv decreased TBARs, but increased the mortality rate, the parasitaemia and the levels of CCL2, CCL5, catalase and the inflammatory infiltrate in the cardiac tissue. Bz led the reduction of the inflammatory infiltrate and circulating levels of oxidative stress and inflammatory mediators in the infected mice. MAIN CONCLUSIONS Our data suggest that Cv, in this experimental model using the Colombian strain of T. cruzi, caused damage to the host.
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    Trypanosoma cruzi antigens induce inflammatory angiogenesis in a mouse subcutaneous sponge model.
    (2015) Silva, Francisca Hildemagna Guedes da; Bajracharya, Deena Shrestha; Salles, Beatriz Cristina Silveira; Figueiredo, Vivian Paulino; Lopes, Laís Roquete; Dias, Luiza; Barcelos, Luciola da Silva; Moura, Sandra Aparecida Lima de; Andrade, Silvia Passos de; Silva, André Talvani Pedrosa da
    Acute inflammation and angiogenesis are persistent features of several pathological conditions induced by biological agents leading to the resolution of local and systemic events. Glycoproteins derived from the protozoan Trypanosoma cruzi are suggested to mediate angiogenesis induced by inflammatory cells with still undescribed mechanisms. In this study, we investigated the effects of total antigen from trypomastigote forms of T. cruzi (Y strain), inoculated in sponges 24 h after implantation inmice, on angiogenesis, inflammatory cell pattern and endogenous production of inflammatory and angiogenicmediators on days 1, 4, 7 and 14 post-implant. There was an increase in hemoglobin content and in the number of blood vessels associated with T. cruzi antigen stimuli on the 14th day, assessed by the hemoglobin of the implants and by morphometric analysis. However, these antigens were not able to increase type I collagen content on the 14th day. Parasite antigens also induced high production of vascular endothelial growth factor (VEGF) and inflammatory mediators TNF-alpha, CCL2 and CCL5 on the 7th day in sponges when compared to the unstimulated group. Neutrophils and macrophages were determined by measuring myeloperoxidase (MPO) and N-acetyl-β-D-glucosaminidase (NAG) enzyme activities, respectively. Only NAG was increased after stimulation with antigens, starting from day 4 and peaking at day 7. Together, these data showed that antigens fromthe Y strain of T. cruzi are able to promote inflammatory neovascularization probably induced by macrophage-induced angiogenic mediators in T. cruzi antigen-stimulated sponges in Swiss mice.