Navegando por Palavras-chave "iNOS"

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    Ascorbic acid prevents acute myocardial infarction induced by isoproterenol in rats: role of inducible nitric oxide synthase production
    (Springer, 2009-04-01) Ribeiro, Daniel Araki [UNIFESP]; Buttros, Juliana Beatriz [UNIFESP]; Oshima, Celina Tizuko Fujiyama [UNIFESP]; Bergamaschi, Cassia Toledo [UNIFESP]; Campos, Ruy Ribeiro [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    The goal of this study was to investigate whether sub-chronic anti-oxidant treatment with ascorbic acid (Vit C) is able to protect the heart against myocardial infarction. the effects of Vit C treatment on the histopatological changes and immunohistochemistry for p53, COX-2 and iNOS were evaluated in rats submitted to acute myocardial infarction induced by isoproterenol (ISO). Male Wistar rats (n = 32) were divided into four groups: group 1, control; group 2, ISO treated; group 3, Vit C treated; group 4, ISO + Vit C treated. An amount of 150 mg/kg of isoproterenol was administered for two consecutive days. the rats were treated with Vit C once a day (150 mg/kg, orally) for seven consecutive days. in the day 5 and 6 the rats from group ISO + Vit C were submitted to acute administration of ISO third minutes after Vit C treatment. the results pointed out that treatment with Vit C showed mild degenerative changes of myocardial tissue in ISO group. Also, the antioxidant was able to decrease the iNOS expression in rats treated with Vit C. Taken together, our results suggest that chronic Vit C administration was able to prevent the myocardial infarction induced by ISO as a result of iNOS downregulation. Certainly, this finding offers new insights into the mechanisms underlying the relation between oxidative stress and cardiac mortality after myocardial infarction.
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    Effect of Concentrated Apple Extract on Experimental Colitis Induced by Acetic Acid
    (Cellular & Molecular Biology Research Center, 2017) Pastrelo, Maurcio Mercaldi [UNIFESP]; Ribeiro, Carla Caroline Dias [UNIFESP]; Duarte, Joselmo Willamys [UNIFESP]; Gollucke, Andrea Pittelli Boiago [UNIFESP]; Artigiani Neto, Ricardo [UNIFESP]; Ribeiro, Daniel Araki [UNIFESP]; Miszputen, Sender Jankiel [UNIFESP]; Oshima, Celina Tizuko Fujiyama [UNIFESP]; Paiotti, Ana Paula Ribeiro [UNIFESP]
    Reactive oxygen and nitrogen species (ROS/RNS) play a crucial role in inflammatory bowel disease (IBD) exacerbating the chronic inflammatory process. Endogenous and diet antioxidants can neutralize these compounds. The apple is widely consumed, with several antioxidant activity compounds. The present study evaluated the effects of concentrated apple extract (CAE) in acetic acid induced colitis. 29 Wistar male rats were randomized into 5 groups. G1-Sham/saline solution, G2-CAE/control, G3-acetic acid/control, G4-curative-CAE treatment and G5-preventive-CAE treatment. Eight days later, the animals were euthanized and the colonic segment resected for macroscopic and histological analysis. Gene expression was evaluated for inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), catalase and copper and zinc superoxide dismutase (CuZnSOD) by quantitative real time PCR, while protein expression was assessed for iNOS, COX-2 and 8-hydroxy-20-deoxyguanosine (8-OHdG) via immunohistochemistry. The groups G3, G4 and G5 had weight loss, while G5 had weight increase at the end of the experiment. The treatment with CAE reduced the macroscopic and microscopic injury, decreased iNOS mRNA expression and increased CuZnSOD mRNA expression in animals with induced acetic acid-colitis. The findings of the present study suggest that CAE treatment exerts an antioxidant role by downregulating iNOS and upregulating CuZnSOD.
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    Effects of corticosteroid, montelukast and iNOS inhibition on distal lung with chronic inflammation
    (Elsevier B.V., 2013-01-15) Ribas Souza, Flavia Castro; Gobbato, Nathalia Brandao; Maciel, Rafaela Guerra; Prado, Carla Maximo [UNIFESP]; Martins, Milton Arruda; Leick, Edna A.; Calvo Tiberio, Iolanda F. L.; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)
    We evaluated the effects of anti-iNOS (1400W - W) associated with leukotriene antagonist (montelukast - M) or corticosteroid (dexamethasone - D) on distal lung of guinea pigs (GP) with chronic pulmonary inflammation.Methods: GP were inhaled with ovalbumin (OVA-2x/week/4 weeks), treated with M (OVAM), D (OVAD) and/or W (OVAW, OVADW, OVAMW) and distal lungs were evaluated by morphometry.Results: Isolated treatments were not sufficient to reduce all parameters. in OVADW, all parameters were reduced with greater reduction in elastic fibers, TIMP-1, IL-4, IL-5, IFN-gamma and PGF2-alpha compared with OVAD (p<0.05). OVAMW potentiated the reduction of actin, elastic fibers, TIMP-1, IL-4, IL-5, TGFbeta, IFN-gamma, iNOS, and PGF2-alpha to a greater extent than OVAM (p<0.05). A reduction of TIMP-1, IL-4, IL-5, TGF-beta, IFN-gamma and iNOS was observed in OVADW compared with OVAMW (p<0.05).Conclusions: Although anti-iNOS paired with montelukast or dexamethasone yields better results than isolated treatments, the most effective pairing for controlling inflammation, oxidative stress and remodeling in this asthma model was found to be corticosteroids and anti-iNOS. (C) 2012 Published by Elsevier B.V.
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    Impairment of male reproductive function after sleep deprivation
    (Elsevier B.V., 2015-05-01) Alvarenga, Tathiana A. [UNIFESP]; Hirotsu, Camila [UNIFESP]; Mazaro-Costa, Renata; Tufik, Sergio [UNIFESP]; Andersen, Monica L. [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Universidade Federal de Goiás (UFG)
    Objective: To evaluate the influence of sleep loss on sexual behavior, hormone levels, sperm parameters, and testis-specific gene expression in male rats.Design: Experimental research.Setting: Animal laboratory.Animal(s): Male adult Wistar-Hannover rats.Intervention(s): Sexually experienced rats were subjected to paradoxic sleep deprivation (PSD) for 96 hours or sleep restriction (SR) for 21 days or kept in their home cage as control (CTRL).Main Outcome Measure(s): Sexual behavior, hormone levels, sperm parameters and expression of stress and nitric oxide-related genes were evaluated.Result(s): PSD significantly decreased sexual behavior compared with the CTRL group, whereas SR had no effect. the PSD group had significantly lower testosterone levels than the CTRL group. Both PSD and SR groups had lower sperm viabilities than the CTRL group. the decrease in the number of live sperm compared with the CTRL group was larger in the PSD group than in the SR group. Regarding testicular gene expression, both PSD and SR led to an increase of iNOS and hydroxysteroid 11 beta-dehydrogenase 1 expressions compared with the CTRL group. These changes were more pronounced in the PSD group. A significant increase in endothelial nitric oxide synthase expression was observed in the PSD groups compared with the CTRL group. No changes were observed in dimethylarginine dimethylaminohydrolase 1 and casein kinase 2 beta-polypeptide expressions.Conclusion(s): Sleep loss can promote marked changes in the male reproductive system of rats, particularly affecting spermatic function in part by interfering in the testicular nitric oxide pathway. (C) 2015 by American Society for Reproductive Medicine.
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    Inducible nitric oxide synthase inhibition attenuates lung tissue responsiveness and remodeling in a model of chronic pulmonary inflammation in guinea pigs
    (Elsevier B.V., 2009-02-28) Starling, Claudia Miranda; Prado, Carla Máximo [UNIFESP]; Leick-Maldonado, Edna Aparecida; Lancas, Tatiana; Reis, Fabiana Gomes; Aristoteles, Luciana Ritha de Cassia Rolim Barbosa; Dolhnikoff, Marisa; Martins, Milton de Arruda; Tiberio, Iolanda de Fátima Lopes Calvo; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)
    We evaluated the influence of iNOS-derived NO on the mechanics, inflammatory, and remodeling process in peripheral lung parenchyma of guinea pigs with chronic pulmonary allergic inflammation. Animals treated or not with 1400W were submitted to seven exposures of ovalbumin in increasing doses. Seventy-two hours after the 7th inhalation, lung strips were suspended in a Krebs organ bath, and tissue resistance and elastance measured at baseline and after ovalbumin challenge. the strips were submitted to histopathological measurements. the ovalbumin-exposed animals showed increased maximal responses of resistance and elastance (p < 0.05), eosinophils counting (p < 0.001), iNOS-positive cells (p < 0.001), collagen and elastic fiber deposition (p < 0.05), actin density (p < 0.05) and 8-iso-PGF2 alpha expression (p < 0.001) in alveolar septa compared to saline-exposed ones. Ovalbumin-exposed animals treated with 1400 W had a significant reduction in lung functional and histopathological findings (p < 0.05). We showed that iNOS-specific inhibition attenuates lung parenchyma constriction, inflammation, and remodeling, suggesting NO-participation in the modulation of the oxidative stress pathway. (C) 2008 Elsevier B.V. All rights reserved.
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    Influence of sleep deprivation and morphine on the expression of inducible nitric oxide synthase and cyclooxygenase-2 in skin of hairless mice
    (Informa Healthcare, 2012-10-01) Egydio, Flavia [UNIFESP]; Ribeiro, Daniel Araki [UNIFESP]; Noguti, Juliana [UNIFESP]; Tufik, Sergio [UNIFESP]; Andersen, Monica Levy [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Skin performs a host of primordial functions that keep the body alive. Morphine is a drug with immunosuppressant properties whose chronic use may lead to increased infection and delayed wound healing. Sleep is a fundamental biological phenomenon that promotes the integrity of several bodily functions. Sleep deprivation adversely affects several systems, particularly the immune system. the aim of this study was to perform an immunohistochemical evaluation on the expression of inducible nitric oxide synthase and cyclooxygenase-2 in skin of sleep-deprived mice and mice chronically treated with morphine. Adult hairless male mice were distributed into the following groups: Control, morphine, sleep-deprived, and morphine + SD. Morphine (10 mg/kg, subcutaneous) was injected every 12 h for 9 days. Morphine induced immunoexpression of cyclooxygenase-2 and nitric oxide synthase. Sleep deprivation did not modulate outcomes induced by morphine. Morphine, not sleep loss, induces cyclooxygenase-2 and nitric oxide synthase immunoexpression in the skin of hairless mice.
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    Modulation of the oscillatory mechanics of lung tissue and the oxidative stress response induced by arginase inhibition in a chronic allergic inflammation model
    (Biomed Central Ltd, 2013-08-15) Aristoteles, Luciana R. C. R. B.; Righetti, Renato F.; Pinheiro, Nathalia Montouro; Franco, Rosana B.; Starling, Claudia M.; Silva, Julie C. P. da; Pigati, Patricia Angeli; Caperuto, Luciana Chagas [UNIFESP]; Prado, Carla Máximo [UNIFESP]; Dolhnikoff, Marisa; Martins, Milton A.; Leick, Edna A.; Tiberio, Iolanda F. L. C.; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)
    Background: the importance of the lung parenchyma in the pathophysiology of asthma has previously been demonstrated. Considering that nitric oxide synthases (NOS) and arginases compete for the same substrate, it is worthwhile to elucidate the effects of complex NOS-arginase dysfunction in the pathophysiology of asthma, particularly, related to distal lung tissue. We evaluated the effects of arginase and iNOS inhibition on distal lung mechanics and oxidative stress pathway activation in a model of chronic pulmonary allergic inflammation in guinea pigs.Methods: Guinea pigs were exposed to repeated ovalbumin inhalations (twice a week for 4 weeks). the animals received 1400 W (an iNOS-specific inhibitor) for 4 days beginning at the last inhalation. Afterwards, the animals were anesthetized and exsanguinated; then, a slice of the distal lung was evaluated by oscillatory mechanics, and an arginase inhibitor (nor-NOHA) or vehicle was infused in a Krebs solution bath. Tissue resistance (Rt) and elastance (Et) were assessed before and after ovalbumin challenge (0.1%), and lung strips were submitted to histopathological studies.Results: Ovalbumin-exposed animals presented an increase in the maximal Rt and Et responses after antigen challenge (p<0.001), in the number of iNOS positive cells (p<0.001) and in the expression of arginase 2, 8-isoprostane and NF-kB (p<0.001) in distal lung tissue. the 1400 W administration reduced all these responses (p<0.001) in alveolar septa. Ovalbumin-exposed animals that received nor-NOHA had a reduction of Rt, Et after antigen challenge, iNOS positive cells and 8-isoprostane and NF-kB (p<0.001) in lung tissue. the activity of arginase 2 was reduced only in the groups treated with nor-NOHA (p <0.05). There was a reduction of 8-isoprostane expression in OVA-NOR-W compared to OVA-NOR (p<0.001).Conclusions: in this experimental model, increased arginase content and iNOS-positive cells were associated with the constriction of distal lung parenchyma. This functional alteration may be due to a high expression of 8-isoprostane, which had a procontractile effect. the mechanism involved in this response is likely related to the modulation of NF-kB expression, which contributed to the activation of the arginase and iNOS pathways. the association of both inhibitors potentiated the reduction of 8-isoprostane expression in this animal model.
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    Papel dos inflamassomas no controle da infecção por Trypanosoma cruzi
    (Universidade Federal de São Paulo, 2013-07-30) Gonçalves, Virginia Mendes [UNIFESP]; Bortoluci, Karina Ramalho [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Demonstramos pela primeira vez que a infecção pelo T. cruzi induz a produção de IL-1β de uma forma dependente NLRP3 e caspase-1. Camundongos NLRP3-/- e caspase1-/-apresentaram um elevado número de parasitas, apresentando picos de parasitemia mais altos do que animais MyD88-/-, indicando o envolvimento do inflamassoma NLRP3 no controle da fase aguda da infecção pelo T. cruzi. As citocinas inflamatórias IL-6 e IFN-γ foram encontradas nas culturas de esplenócitos de NLRP3-/- e caspase1-/- infectados com T. cruzi. Porém essas células apresentaram uma deficiência na produção de óxido nítrico (NO), que reflete na permissividade de seus macrófagos à replicação do T. cruzi. Curiosamente, a inibição da caspase-1, z-YVAD-fmk, mas não a presença do antagonista de IL-1R (IL-1Ra) aboliram a produção de NO em macrófagos WT e MyD88-/ - e os tornaram mais susceptíveis como as células do NLRP3-/ - e caspase-1-/-. Além disso, a catepsina B parece ser necessária para a ativação de NLRP3 em resposta ao T. cruzi, uma vez que a sua inibição farmacológica aboliu a secreção de IL-1β e NO. Tomados em conjunto os nossos resultados demonstram o papel do inflamassoma NLRP3 no controle da infecção pelo T. cruzi, demonstrando que NLRP3, por uma via dependente de caspase-1 e independente de IL-1R, induz a produção de NO, atribuindo um novo mecanismo efetor para estes receptores.