Navegando por Palavras-chave "Annexin A1"
Agora exibindo 1 - 5 de 5
Resultados por página
Opções de Ordenação
- ItemSomente MetadadadosAC(2-26) peptide and serine protease of Bothrops atrox similarly induces angiogenesis without triggering local and systemic inflammation in a murine model of dorsal skinfold chamber(Pergamon-Elsevier Science Ltd, 2017) Molas, Rafaela Batista; de Paula-Silva, Marina; Masood, Rehana; Ullah, Anwar; Gimenes, Alexandre Dantas [UNIFESP]; Oliani, Sonia Maria [UNIFESP]
- ItemSomente MetadadadosAnnexin A1 protein attenuates cyclosporine-induced renal hemodynamics changes and macrophage infiltration in rats(Springer, 2012-03-01) Araujo, Leandro Pires [UNIFESP]; Truzzi, Renata Ramos; Florido Mendes, Gloria Elisa; Mendes Luz, Marcus Alexandre; Burdmann, Emmanuel A.; Oliani, Sonia Maria [UNIFESP]; São Paulo State Univ UNESP; Universidade Federal de São Paulo (UNIFESP); Sao Jose do Rio Preto Med Sch; Universidade de São Paulo (USP)Cyclosporine (CsA) remains an important immunosuppressant for transplantation and for treatment of autoimmune diseases. the most troublesome side effect of CsA is renal injury. Acute CsA-induced nephrotoxicity is characterized by reduced renal blood flow (RBF) and glomerular filtration rate (GFR) due to afferent arteriole vasoconstriction. Annexin A1 (ANXA1) is a potent anti-inflammatory protein with protective effect in renal ischemia/reperfusion injury. Here we study the effects of ANXA1 treatment in an experimental model of acute CsA nephrotoxicity.Salt-depleted rats were randomized to treatment with VH (vehicles 1 mL/kg body weight/day), ANXA1 (Ac2-26 peptide 1 mg/kg body weight/day intraperitoneally), CsA (20 mg/kg body weight/day subcutaneously) and CsA + ANXA1 (combination) for seven days. We compared renal function and hemodynamics, renal histopathology, renal tissue macrophage infiltration and renal ANXA1 expression between the four groups.CsA significantly impaired GFR and RBF, caused tubular dilation and macrophage infiltration and increased ANXA1 renal tissue expression. Treatment with ANXA1 attenuated CSA-induced hemodynamic changes, tubular injury and macrophage infiltration.ANXA1 treatment attenuated renal hemodynamic injury and inflammation in an acute CsA nephrotoxicity model.
- ItemSomente MetadadadosInteraction of the Anti-Inflammatory Annexin A1 Protein and Tacrolimus Immunosuppressant in the Renal Function of Rats(Karger, 2010-01-01) Araujo, Leandro P. [UNIFESP]; Truzzi, Renata R.; Mendes, Gloria E.; Luz, Marcus A. M.; Burdmann, Emmanuel A.; Oliani, Sonia M. [UNIFESP]; UNESP; Universidade Federal de São Paulo (UNIFESP); Universidade de São Paulo (USP)Background: Tacrolimus (FK) is currently widely used in transplant immunosuppression and the treatment of autoimmune diseases. However, FK induces nephrotoxicity which is characterized by functional and structural renal injury. the ubiquitous protein annexin A1 (ANXA1) has potent anti-inflammatory effects and protects against ischemia/reperfusion injury. We investigated the effects of exogenous ANXA1 treatment in an experimental model of acute FK nephrotoxicity. Methods: Munich-Wistar rats received a low-salt diet for 1 week and were randomized to treatment with ANXA1 (Ac2-26 peptide 0.5 mg/kg/day s.c.), FK (6 mg/kg/day p.o.), association (FK+ANXA1) and vehicles (1 ml/kg/day) for 7 days. Results: FK induced a significant decrease in glomerular filtration rate and renal blood flow, and a significant increase in renal vascular resistance. in addition, FK caused extensive acute tubule-interstitial damage and an increase in anti-inflammatory ANXA1 expression in renal tissue. Exogenous ANXA1 treatment reduced FK-induced tubular dilatation and macrophage infiltration. for the first time, we observed that FK augmented ANXA1 expression in renal tissue. Conclusion: Exogenous ANXA1 treatment partially protected against FK-induced tubular injury and macrophage infiltration, and may be targeted in renal intervention strategies. Copyright (C) 2010 S. Karger AG, Basel
- ItemSomente MetadadadosRole of the protein annexin A1 on the efficacy of anti-TNF treatment in a murine model of acute colitis(Pergamon-Elsevier Science Ltd, 2016) de Paula-Silva, Marina [UNIFESP]; Elisabeth Barrios, Bibiana; Maccio-Maretto, Lisa; Sena, Angela Aparecida; Farsky, Sandra Helena Poliselli; Graciela Correa, Silvia; Oliani, Sonia Maria [UNIFESP]TNF-alpha is involved in the mechanisms that initiate inflammatory bowel diseases (IBDs). Anti-TNF-alpha drugs, such as infliximab (IFX), cause non-responsiveness and side effects, indicating the need to investigate alternative therapies for these diseases. The anti-inflammatory protein, annexin A1 (AnxA1), has been associated with the protection of the gastrointestinal mucosa. To further address the role of endogenous AnxA1 on the TNF-alpha blockade efficacy in a murine model, we assessed colitis induced by Dextran Sulfate Sodium (DSS) in wild-type (WT) and ArucA1(-/-) Balb/c mice treated with IFX. We consistently observed endogenous AnxA1 prevented clinical and physiological manifestations of experimental colitis treated with IFX, additionally the manifestation of the disease was observed earlier in AnxA1(-/-) mice. Rectal bleeding, diarrhea, histological score, epithelial damages and collagen degradation caused by DSS were prevented following IFX treatment only in WT mice. IL-6 increased during colitis in WT and AnxA1(-/-) mice, decreasing under IFX treatment in WT. The influx of neutrophils and TNF-alpha secretion were largely elevated in AnxA1(-/-) mice when compared to WT mice. In the group WT/DSS + IFX, phagocytes were more susceptible to apoptosis following treatment with IFX. Endogenous expression of AnxA1 increased after DSS and decreased with IFX treatment, demonstrating an attenuated inflammatory response. The data indicate that AnxA1 contributes to the establishment of intestinal homeostasis after blocking of TNF-alpha was used as a treatment of IBD, constituting a key molecule in the mechanism of action and a potential biomarker of therapeutic efficacy. (C) 2016 Elsevier Inc. All rights reserved.
- ItemSomente MetadadadosTargeting formyl peptide receptor 2 reduces leukocyte-endothelial interactions in a murine model of stroke(Federation Amer Soc Exp Biol, 2015-05-01) Smith, Helen K.; Gil, Cristiane Damas [UNIFESP]; Oliani, Sonia M. [UNIFESP]; Gavins, Felicity N. E.; Louisiana State Univ; Univ London Imperial Coll Sci Technol & Med; Universidade Federal de São Paulo (UNIFESP)Ischemia/reperfusion (I/R) injury following stroke can worsen patient outcome through excess inflammation. This study investigated the pharmacologic potential of targeting an endogenous anti-inflammatory circuit via formyl peptide receptor (FPR) 2/lipoxin receptor (ALX) (Fpr2/3 in mouse) in global cerebral I/R. Mice (C57BL/6 and Fpr2/3(-/-)) were subjected to bilateral common carotid artery occlusion, followed by reperfusion and treatment with FPR agonists: AnxA1(Ac2-26) [Annexin A1 mimetic peptide (Ac-AMVSEFLKQAWFIENEEQEYVQTVK), 2.5 mu/kg] and 15-epimer-lipoxin A4 (15-epi-LXA(4); FPR2/ALX specific, 12.5 and 100 ng/kg). Leukocyte-endothelial (L-E) interactions in the cerebral microvasculature were then quantified in vivo using intravital fluorescence microscopy. 15-epi-LXA(4) administration at the start of reperfusion reduced L-E interactions after 40 min (which was sustained at 2 h with high-dose 15-epi-LXA(4)) to levels seen in sham-operated animals. AnxA1(Ac2-26) treatment decreased leukocyte adhesion at 40 min and all L-E interactions at 2 h (up to 95%). Combined treatment with AnxA1(Ac2-26) plus FPR antagonists t-Boc-FLFLF (250 ng/kg) or WRW4 (FPR2/ALX selective, 1.4 mu/kg) abrogated the effects of AnxA1(Ac2-26) fully at 40 min. Antagonists were less effective at 2 h, which we demonstrate is likely because of their impact on early L-E interactions. Our findings indicate that FPR2/ALX activity elicits considerable control over vascular inflammatory responses during cerebral I/R and, therefore, provide evidence that targeting FPR2/ALX may be beneficial for patients who suffered from stroke.