TABATA MARUYAMA DOS SANTOS

(Fonte: Lattes)
Índice h a partir de 2011
5
Projetos de Pesquisa
Unidades Organizacionais
LIM/20 - Laboratório de Terapêutica Experimental, Hospital das Clínicas, Faculdade de Medicina

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Agora exibindo 1 - 3 de 3
  • article 0 Citação(ões) na Scopus
    Investigating the Effects of a New Peptide, Derived from the Enterolobium contortisiliquum Proteinase Inhibitor (EcTI), on Inflammation, Remodeling, and Oxidative Stress in an Experimental Mouse Model of Asthma-Chronic Obstructive Pulmonary Disease Overlap (ACO)
    (2023) BARBOSA, Jessica Anastacia Silva; SILVA, Luana Laura Sales da; JOAO, Juliana Morelli Lopes Goncalves; CAMPOS, Elaine Cristina de; FUKUZAKI, Silvia; CAMARGO, Leandro do Nascimento; SANTOS, Tabata Maruyama dos; SANTOS, Henrique Tibucheski dos; BEZERRA, Suellen Karoline Moreira; SARAIVA-ROMANHOLO, Beatriz Mangueira; LOPES, Fernanda Degobbi Tenorio Quirino dos Santos; BONTURI, Camila Ramalho; OLIVA, Maria Luiza Vilela; LEICK, Edna Aparecida; RIGHETTI, Renato Fraga; TIBERIO, Iolanda de Fatima Lopes Calvo
    The synthesized peptide derived from Enterolobium contortisiliquum (pep3-EcTI) has been associated with potent anti-inflammatory and antioxidant effects, and it may be a potential new treatment for asthma-COPD overlap-ACO). Purpose: To investigate the primary sequence effects of pep3-EcTI in an experimental ACO. BALB/c mice were divided into eight groups: SAL (saline), OVA (ovalbumin), ELA (elastase), ACO (ovalbumin + elastase), ACO-pep3-EcTI (treated with inhibitor), ACO-DX (treated with dexamethasone), ACO-DX-pep3-EcTI (treated with dexamethasone and inhibitor), and SAL-pep3-EcTI (saline group treated with inhibitor). We evaluated the hyperresponsiveness to methacholine, exhaled nitric oxide, bronchoalveolar lavage fluid (BALF), mean linear intercept (Lm), inflammatory markers, tumor necrosis factor (TNF-alpha), interferon (IFN)), matrix metalloproteinases (MMPs), growth factor (TGF-beta), collagen fibers, the oxidative stress marker inducible nitric oxide synthase (iNOS), transcription factors, and the signaling pathway NF-kappa B in the airways (AW) and alveolar septa (AS). Statistical analysis was conducted using one-way ANOVA and t-tests, significant when p < 0.05. ACO caused alterations in the airways and alveolar septa. Compared with SAL, ACO-pep3-EcTI reversed the changes in the percentage of resistance of the respiratory system (%Rrs), the elastance of the respiratory system (%Ers), tissue resistance (%Gtis), tissue elastance (%Htis), airway resistance (%Raw), Lm, exhaled nitric oxide (ENO), lymphocytes, IL-4, IL-5, IL-6, IL-10, IL-13, IL-17, TNF-alpha, INF-gamma, MMP-12, transforming growth factor (TGF)-beta, collagen fibers, and iNOS. ACO-DX reversed the changes in %Rrs, %Ers, %Gtis, %Htis, %Raw, total cells, eosinophils, neutrophils, lymphocytes, macrophages, IL-1 beta, IL-6, IL-10, IL-13, IL-17, TNF-alpha, INF-gamma, MMP-12, TGF-beta, collagen fibers, and iNOS. ACO-DX-pep3-EcTI reversed the changes, as was also observed for the pep3-EcTI and the ACO-DX-pep3-EcTI. Significance: The pep3-EcTI was revealed to be a promising strategy for the treatment of ACO, asthma, and COPD.
  • article 2 Citação(ões) na Scopus
    Effects of a Peptide Derived from the Primary Sequence of a Kallikrein Inhibitor Isolated from Bauhinia bauhinioides (pep-BbKI) in an Asthma-COPD Overlap (ACO) Model
    (2023) SILVA, Luana Laura Sales da; BARBOSA, Jessica Anastacia Silva; JOAO, Juliana Morelli Lopes Goncalves; FUKUZAKI, Silvia; CAMARGO, Leandro do Nascimento; SANTOS, Tabata Maruyama dos; CAMPOS, Elaine Cristina de; COSTA, Arthur Silva; SARAIVA-ROMANHOLO, Beatriz Mangueira; BEZERRA, Suellen Karoline Moreira; LOPES, Fernanda Tenorio Quirino dos Santos; BONTURI, Camila Ramalho; OLIVA, Maria Luiza Vilela; LEICK, Edna Aparecida; RIGHETTI, Renato Fraga; TIBERIO, Iolanda de Fatima Lopes Calvo
    (1) There are several patients with asthma-COPD overlap (ACO). A peptide derived from the primary sequence of a kallikrein inhibitor isolated from Bauhinia bauhinioides (pep-BbKI) has potent anti-inflammatory and antioxidant effects. Purpose: To investigate the effects of pep-BbKI treatment in an ACO model and compare them with those of corticosteroids. (2) BALB/c mice were divided into groups: SAL (saline), OVA (ovalbumin), ELA (elastase), ACO (ovalbumin + elastase), ACO-pep-BbKI (treated with inhibitor), ACO-DX (dexamethasone treatment), ACO-DX-pep-BbKI (both treatments), and SAL-pep-BbKI (saline group treated with inhibitor). We evaluated: hyperresponsiveness to methacholine, bronchoalveolar lavage fluid (BALF), exhaled nitric oxide (eNO), IL-1 & beta;, IL-4, IL-5, IL-6, IL-10, IL-13, IL-17, IFN-& gamma;, TNF-& alpha;, MMP-9, MMP-12, TGF-& beta;, collagen fibers, iNOS, eNO, linear mean intercept (Lm), and NF-& kappa;B in airways (AW) and alveolar septa (AS). (3) ACO-pep-BbKI reversed ACO alterations and was similar to SAL in all mechanical parameters, Lm, neutrophils, IL-5, IL-10, IL-17, IFN-& gamma;, TNF-& alpha;, MMP-12 (AW), collagen fibers, iNOS (AW), and eNO (p > 0.05). ACO-DX reversed ACO alterations and was similar to SAL in all mechanical parameters, Lm, total cells and differentials, IL-1 & beta;(AS), IL-5 (AS), IL-6 (AS), IL-10 (AS), IL-13 (AS), IFN-& gamma;, MMP-12 (AS), TGF-& beta; (AS), collagen fibers (AW), iNOS, and eNO (p > 0.05). SAL was similar to SAL-pep-BbKI for all comparisons (p > 0.05). (4) Pep-BbKI was similar to dexamethasone in reducing the majority of alterations of this ACO model.
  • article 3 Citação(ões) na Scopus
    Modulating asthma-COPD overlap responses with IL-17 inhibition
    (2023) CAMARGO, Leandro do Nascimento; RIGHETTI, Renato Fraga; ALMEIDA, Francine Maria de; SANTOS, Tabata Maruyama dos; FUKUZAKI, Silvia; MARTINS, Nilo Arthur Bezerra; BARBEIRO, Miguel Cantadori; SARAIVA-ROMANHOLO, Beatriz Mangueira; LOPES, Fernanda Degobbi Tenorio Quirino dos Santos; LEICK, Edna Aparecida; PRADO, Carla Maximo; TIBERIO, Iolanda de Fatima Lopes Calvo
    Background: IL-17 is a modulator of the inflammatory response and is implicated in lung remodeling in both asthma and chronic obstructive pulmonary disease (COPD). Well as and probably in patients with asthma-COPD overlap (ACO).Methods: In this study, we evaluated the response of the airways and alveolar septa to anti-IL-17 treatment in an ACO model. Fifty-six male BALB/c mice were sensitized with ovalbumin (OVA group), received porcine pancreatic elastase (PPE group), or both (ACO group). Mice were then treated with either anti-IL-17 monoclonal antibody or saline. We evaluated hyperresponsiveness, bronchoalveolar lavage fluid (BALF) cell counts, and mean alveolar diameter. We quantified inflammatory, response, extracellular matrix remodeling, oxidative stress markers, and signaling pathway markers.Results: Anti-IL-17 treatment in the ACO anti-IL-17 group reduced the maximum response of respiratory system Rrs, Ers, Raw, Gtis, this when compared to the ACO group (p<0.05). There was a reduction in the total number of inflammatory cells, neutrophils, and macrophages in the BALF in the ACO anti-IL-17 group compared to the ACO group (p<0.05). There was attenuated dendritic cells, CD4+, CD8+, FOXP3, IL-1 beta, IL-2, IL-6, IL-13, IL-17, IL-33 in ACO anti-IL-17 group in airway and alveolar septum compared to the ACO group (p<0.05). We observed a reduction of MMP-9, MMP-12, TIMP-1, TGF-beta, collagen type I in ACO anti-IL-17 group in airway and alveolar septum compared to the ACO group (p < 0.05). We also observed a reduction of iNOS and 8-iso-PGF2 alpha in the airways and in the alveolar septum was reduced in the ACO anti-IL-17group compared to the ACO group (p < 0.05). Regarding the signaling pathways, NF-kB, ROCK-1, and ROCK-2 in the airway and alveolar septum were attenuated in the ACO anti-IL-17 group when compared to the ACO group (p<0.05).Conclusions: Our results suggest that inhibiting IL-17 modulates cell-associated cytokine production in lung tissue, extracellular matrix remodeling, and oxidative stress in ACO through the modulation of NF-kB and FOXP3.