AURELIO CANABRAVA GARRIDO

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LIM/20 - Laboratório de Terapêutica Experimental, Hospital das Clínicas, Faculdade de Medicina

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  • conferenceObject
    Anti-IL17 treatment control responses in lung injury induced by elastase
    (2018) FUKUZAKI, Silvia; GARRIDO, Aurelio C.; RIGHETTI, Renato F.; SANTOS, Tabata M.; CAMARGO, Leandro N.; ARISTOTELES, Luciana R. C. R. B.; SOUZA, Flavia C. R.; SARAIVA-ROMANHOLO, Beatriz M.; LEICK, Edna A.; PRADO, Carla M.; MARTINS, Milton A.; TIBERIO, Iolanda F. L. C.
  • conferenceObject
    Inflammation and remodeling modulated by anti IL17 in model of lung injury induced by elastase in mice
    (2019) LEICK, Edna A.; FUKUZAKI, Silvia; RIGHETTI, Renato F.; SANTOS, Tabata M.; CAMARGO, Leandro N.; GARRIDO, Aurelio C.; ARISTOTELES, Luciana R. C. R. B.; SOUZA, Flavia C. R.; SARAIVA-ROMANHOLO, Beatriz M.; PRADO, Carla M.; MARTINS, Milton A.; TIBERIO, Iolanda F. L. C.
  • article 7 Citação(ões) na Scopus
    Preventive and therapeutic effect of anti-IL-17 in an experimental model of elastase-induced lung injury in C57Bl6 mice
    (2021) FUKUZAKI, Silvia; RIGHETTI, Renato Fraga; SANTOS, Tabata Maruyama dos; CAMARGO, Leandro do Nascimento; ARISTOTELES, Luciana R. C. R. B.; SOUZA, Flavia C. R.; GARRIDO, Aurelio C.; SARAIVA-ROMANHOLO, Beatriz Mangueira; LEICK, Edna Aparecida; PRADO, Carla Maximo; MARTINS, Milton de Arruda; TIBERIO, Iolanda de Fatima Lopes Calvo
    Chronic obstructive pulmonary disease (COPD) is an important health care issue, and IL-17 can modulate inflammatory responses. We evaluated preventive and therapeutic effect of anti-interleukin (IL)-17 in a model of lung injury induced by elastase, using 32 male C57Bl6 mice, divided into 4 groups: SAL, ELASTASE CONTROL (EC), ELASTASE I PREVENTIVE ANTI-IL-17 (EP), and ELASTASE + THERAPEUTIC ANTI-IL-17 (ET). On the 29th day, animals were anesthetized with thiopental, tracheotomized, and placed on a ventilator to evaluate lung mechanical, exhaled nitric oxide (eNO), and total cells of bronchoalveolar lavage fluid was collected. We performed histological techniques, and linear mean intercept (Lm) was analyzed. Both treatments with anti-IL-17 decreased respiratory resistance and elastance, airway resistance, elastance of pulmonary parenchyma, eNO, and Lm compared with EC. There was reduction in total cells and macrophages in ET compared with EC. Both treatments decreased nuclear factor-kappa B, inducible nitric oxide synthase, matrix metalloproteinase (MMP)-9, MMP-12, transforming growth factor-beta, tumor necrosis factor-alpha, neutrophils, IL-1 beta, isoprostane, and IL-17 in airways and alveolar septa; collagen fibers, decorin and lumican in airways; and elastic fibers and fibronectin in alveolar septa compared with EC. There was reduction of collagen fibers in alveolar septa and biglycan in airways in EP and a reduction of eNO synthase in airways in ET. In conclusion, both treatments with anti-IL-17 contributed to improve most of parameters evaluated in inflammation and extracellular matrix remodeling in this model of lung injury.