Navegando por Autor "Valença, Samuel dos Santos"

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Estudo dos efeitos da Hesperidina em células e camundongos submetidos à ventilação mecânica.
(2022) Souza, Ana Beatriz Farias de; Bezerra, Frank Silva; Menezes, Rodrigo Cunha Alvim de; Bezerra, Frank Silva; Valença, Samuel dos Santos; Silva, Pedro Leme; Vieira, Paula Melo de Abreu; Souza, Gustavo Henrique Bianco de; Menezes, Rodrigo Cunha Alvim de
A ventilação mecânica (VM) é uma ferramenta utilizada na assistência ao paciente crítico, porém pode desencadear processos inflamatórios e oxidativos capazes de causar ou agravar lesões pulmonares. A hesperidina é um flavonoide encontrado em frutas cítricas que apresenta propriedades antioxidantes e anti-inflamatórias. Este estudo teve como objetivo avaliar os efeitos da administração de hesperidina em células e camundongos submetidos à VM. O estudo foi dividido em ensaios in vitro e in vivo, inicialmente foi avaliado os efeitos in vitro da hesperidina. Utilizando diferentes concentrações de hesperidina (12,21; 24,42; 48,84; 97,7; 195,4 μg/mL) e lipopolissacarídeo (LPS) (0,25; 0,5; 1,0; 2,0; 4,0 μg/mL) avaliamos em macrófagos da linhagem J774A.1 por meio do teste de MTT alterações na viabilidade celular e, posteriormente utilizando as melhores concentrações e hesperidina e LPS foi avaliada a produção intracelular de espécies reativas de oxigênio (ERO). Para os ensaios in vivo foram utilizados 50 camundongos C57BL/6 com idade entre 7 e 8 semanas. Os animais foram divididos em 2 ensaios (n = 25), e para ambos experimentos os camundongos foram randomizados em 5 grupos: grupo controle (GC), grupo ventilação mecânica (GVM), grupo VM + hesperidina 10 mg/kg (VMH10), grupo VM + hesperidina 25 mg/kg (VMH25) e grupo VM + hesperidina 50 mg/kg (VMH50). Os animais receberam solução salina (GC e GVM) ou solução de hesperidina (VMH10, VMH25 e VMH50) via gavagem orogástrica, sendo que para o primeiro ensaio a administração das soluções ocorreu seis horas antes do início da VM, já para o segundo estudo os animais receberam as respectivas soluções por 30 dias consecutivos antes do início da VM. Em ambos ensaios após o tempo de administração das soluções os animais foram submetidos à VM no modo controlado à volume por uma hora utilizando os seguintes parâmetros: volume corrente de 10 mL/kg, fração inspirada de oxigênio de 21%, frequência respiratória de 150 incursões respiratórias por minuto e pressão positiva ao final da expiração de 2 cmH2O. Ao término da VM os animais foram eutanasiados e foram coletados sangue, lavado broncoalveolar (LBA) e pulmões. No ensaio in vitro, células expostas por 24 horas à hesperidina, nas concentrações de 24,42; 48,85; 97,7 e 195.4 μg/mL apresentaram aumento da viabilidade celular quando comparado com o controle. Além disso, as células que foram incubadas com hesperidina (24,42; 48,85 e 97,7 μg/mL) e LPS (1,0 μg/mL) apresentaram menor produção de ERO quando comparado com as células expostas apenas ao LPS. Para os ensaios in vivo, os animais receberam a hesperidina seis horas antes do início da VM, especialmente os grupos VMH25 e VMH50, apresentaram menor influxo de células inflamatórias para as vias aéreas e menor dano oxidativo, quando comparado com GVM. Além disso, a administração de hesperidina modulou a resposta inflamatória, reduzindo os níveis de CLL2 e IL-12. A administração da hesperidina por trinta dias antes do início da VM promoveu em todas as doses utilizadas, uma diminuição do influxo de células inflamatórias, dano oxidativo e nos níveis de CCL2, TNF-α e IL-12. Em conclusão, a administração de única ou múltiplas doses de hesperidina exerceu efeitos protetivos sobre os pulmões de camundongos submetidos à ventilação mecânica.
Long-term exposure to cigarette smoke impairs lung function and increases HMGB-1 expression in mice.
(2011) Bezerra, Frank Silva; Valença, Samuel dos Santos; Pires, Karla Maria Pereira; Lanzetti, Manuella; Pimenta, Wagner Alves; Schmidt, Aline Cunha; Porto, Luís Cristovão de Moraes Sobrino; Zin, Walter Araújo
Cigarette smoke (CS)-induced emphysema is caused by a continuous inflammatory response in the lower respiratory tract. The development of the condition is believed to be mediated by oxidant–antioxidant imbalance. This paper describes the effects of long-term CS exposure on alveolar cell recruitment, antioxidant defense systems, activity of extracellular matrix metalloelastases, expression of metalloelastase MMP-12, and high mobility group box-1 protein (HMGB-1). Ten C57Bl/6 mice were exposed to 12 cigarettes-a-day for 60 consecutive days, while 10 control animals were exposed to ambient air. After sacrifice, bronchoalveolar lavage fluid (BALF) was removed, and lung tissue underwent biochemical and histological analyses. In CS-exposed animals influx of alveolar macrophages and neutrophils into BALF, lung static elastance, and expression of MMP-12 and HMGB-1 were significantly increased while the activity of antioxidant enzyme was significantly reduced in comparison with control group. Thus, we demonstrated for the first time that long-term CS exposure decreased antioxidant defenses concomitantly with impaired lung function, which was associated with HMGB-1 expression.
N-(2-mercaptopropionyl)-glycine but not Allopurinol prevented cigarette smoke-induced alveolar enlargement in mouse.
(2011) Pires, Karla Maria Pereira; Bezerra, Frank Silva; Machado, Mariana Nascimento; Zin, Walter Araújo; Porto, Luís Cristovão de Moraes Sobrino; Valença, Samuel dos Santos
We investigated the possible protective effects of the Allopurinol (A), N-(2-mercaptopropionyl)-glycine (M) and N-acetylcysteine (N) against lung injury caused by long-term exposure to cigarette smoke (CS) in mouse. C57BL6 mice were exposed to 12 cigarettes a day for 60 days and concomitantly treated with either one of the antioxidant drugs diluted in saline (CS + A—50 mg/kg; CS + M—200 mg/kg/day; CS + N—200 mg/kg/day). Control groups were sham-smoked (AA). Long-term CS exposure results in extensive parenchyma destruction in CS group. Both CS + N and CS + M groups showed preserved alveolar structure and showed preserved lung function when compared to CS group. Macrophage and neutrophil counts were decreased in CS + M, and CS + N groups when compared to CS group (p < 0.05). Antioxidant enzyme activities were reduced in all treated groups. CS + A showed the highest reduction in catalase activity (−25%, p < 0.01). We conclude that M treatment reduced long-term CS-induced inflammatory lung parenchyma destruction and lung function, comparable to N treatment, however, antioxidant administration did not reverse CS-induced antioxidant enzyme activity reduction.
Oxidative stress and inflammation in acute and chronic lung injuries.
(2023) Bezerra, Frank Silva; Lanzetti, Manuella; Nesi, Renata Tiscoski; Nagato, Akinori Cardozo; Silva, Cyntia Pecli e; Feitosa, Emanuel Kennedy; Melo, Adriana Correa; Cavalieri, Isabella Cattani; Porto, Luís Cristovão de Moraes Sobrino; Valença, Samuel dos Santos
Acute and chronic lung injuries are among the leading causes of mortality worldwide. Lung injury can affect several components of the respiratory system, including the airways, parenchyma, and pulmonary vasculature. Although acute and chronic lung injuries represent an enormous economic and clinical burden, currently available therapies primarily focus on alleviating disease symptoms rather than reversing and/or preventing lung pathology. Moreover, some supportive interventions, such as oxygen and mechanical ventilation, can lead to (further) deterioration of lung function and even the development of permanent injuries. Lastly, sepsis, which can originate extrapulmonary or in the respiratory system itself, contributes to many cases of lung-associated deaths. Considering these challenges, we aim to summarize molecular and cellular mechanisms, with a particular focus on airway inflammation and oxidative stress that lead to the characteristic pathophysiology of acute and chronic lung injuries. In addition, we will highlight the limitations of current therapeutic strategies and explore new antioxidant-based drug options that could potentially be effective in managing acute and chronic lung injuries.
Quantitative and morphological analyses of different types of human liver.
(2011) Nagato, Akinori Cardozo; Silva, Marco Aurélio dos Santos; Trajano, Eduardo Tavares Lima; Alves, Jackson Nogueira; Bandeira, Ana Carla Balthar; Ferreira, Tereza Aparecida; Valença, Samuel dos Santos; Bezerra, Frank Silva
Morphological variations in the human liver have been classified as congenital or acquired, although some may result from pseudo-injuries incurred during medical investigation. The present study comprises a systematic analysis of the anatomical variations exhibited by 61 formalinised and glycerinated adult human livers derived from a collection maintained at the Institute of Anatomy, Universidade Severino Sombra, Vassouras, RJ, Brazil. The vast majority of the organs analysed could be classified according to the seven morphological liver types previously established, although two additional liver types were identified and described. Detailed knowledge of anatomical variations in the human liver could be valuable in improving diagnostic procedures and in attaining a better understanding of pathological conditions associated with some liver diseases
Time course of inflammation, oxidative stress and tissue damage induced by hyperoxia in mouse lungs.
(2012) Nagato, Akinori Cardozo; Bezerra, Frank Silva; Lanzetti, Manuella; Lopes, Alan de Aguiar; Silva, Marco Aurélio dos Santos; Porto, Luís Cristovão de Moraes Sobrino; Valença, Samuel dos Santos
In this study our aim was to investigate the time courses of inflammation, oxidative stress and tissue damage after hyperoxia in the mouse lung. Groups of BALB⁄ c mice were exposed to 100% oxygen in a chamber for 12, 24 or 48 h. The controls were subjected to normoxia. The results showed that IL-6 increased progressively after 12 (P < 0.001) and 24 h (P < 0.001) of hyperoxia with a reduction at 48 h (P < 0.01), whereas TNF-a increased after 24 (P < 0.001) and 48 h (P < 0.001). The number of macrophages increased after 24 h (P < 0.001), whereas the number of neutrophils increased after 24 h (P < 0.01) and 48 h (P < 0.001). Superoxide dismutase activity decreased in all groups exposed to hyperoxia (P < 0.01). Catalase activity increased only at 48 h (P < 0.001). The reduced glutathione ⁄ oxidized glutathione ratio decreased after 12 h (P < 0.01) and 24 h (P < 0.05). Histological evidence of lung injury was observed at 24 and 48 h. This study shows that hyperoxia initially causes an inflammatory response at 12 h, resulting in inflammation associated with the oxidative response at 24 h and culminating in histological damage at 48 h. Knowledge of the time course of inflammation and oxidative stress prior to histological evidence of acute lung injury can improve the safety of oxygen therapy in patients.