Navegando por Palavras-chave "Ischemia-reperfusion"
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- ItemAcesso aberto (Open Access)Contribution of CD4+ T cells to the early mechanisms of ischemia- reperfusion injury in a mouse model of acute renal failure(Associação Brasileira de Divulgação Científica, 2007-04-01) Pinheiro, Helady Sanders [UNIFESP]; Câmara, Niels Olsen Saraiva [UNIFESP]; Noronha, Irene Lourdes; Longo-Maugéri, Ieda Maria [UNIFESP]; Franco, Marcello Fabiano de [UNIFESP]; Medina, J.o.a.p. [UNIFESP]; Pacheco-Silva, Alvaro [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Universidade Federal de Juiz de Fora Divisão de Nefrologia; Universidade de São Paulo (USP)Renal ischemia-reperfusion (IR) injury is the major cause of acute renal failure in native and transplanted kidneys. Mononuclear leukocytes have been reported in renal tissue as part of the innate and adaptive responses triggered by IR. We investigated the participation of CD4+ T lymphocytes in the pathogenesis of renal IR injury. Male mice (C57BL/6, 8 to 12 weeks old) were submitted to 45 min of ischemia by renal pedicle clamping followed by reperfusion. We evaluated the role of CD4+ T cells using a monoclonal depleting antibody against CD4 (GK1.5, 50 µ, ip), and class II-major histocompatibility complex molecule knockout mice. Both CD4-depleted groups showed a marked improvement in renal function compared to the ischemic group, despite the fact that GK1.5 mAb treatment promoted a profound CD4 depletion (to less than 5% compared to normal controls) only within the first 24 h after IR. CD4-depleted groups presented a significant improvement in 5-day survival (84 vs 80 vs 39%; antibody treated, knockout mice and non-depleted groups, respectively) and also a significant reduction in the tubular necrosis area with an early tubular regeneration pattern. The peak of CD4-positive cell infiltration occurred on day 2, coinciding with the high expression of ßC mRNA and increased urea levels. CD4 depletion did not alter the CD11b infiltrate or the IFN-g and granzyme-B mRNA expression in renal tissue. These data indicate that a CD4+ subset of T lymphocytes may be implicated as key mediators of very early inflammatory responses after renal IR injury and that targeting CD4+ T lymphocytes may yield novel therapies.
- ItemAcesso aberto (Open Access)Estudo do pré-tratamento com atenolol na musculatura cardíaca de ratos submetidos à isquemia-reperfusão intestinal: análise histológica e bioquímica(Universidade Federal de São Paulo (UNIFESP), 2016-10-31) Okada, Aparecida Mieko [UNIFESP]; Oliveira Junior, Itamar Souza de [UNIFESP]; http://lattes.cnpq.br/0568989035666759; http://lattes.cnpq.br/8395419903180596; Universidade Federal de São Paulo (UNIFESP)Purpose: Inflammation has been shown to induce cardiac damage in multiple cardiovascular diseases produced by various insults, including intestinal ischemia-reperfusion. The protective role of atenolol, a beta-1-selective blocker, in myocardial damage after intestinal ischemia/reperfusion is not well understood. Objective: The aim of this study was to evaluate the effects of atenolol as possible cytoprotective drug in myocardial injury by intestinal ischemia - reperfusion in rat model. Materials: Rats were randomly exposed to sham operation, the groups are divided in intestinal ischemia/reperfusion (IR), with saline solution (SS) infusion (SS+IR), and atenolol (AT) infusion and intestinal IR (AT+IR) using atenolol in one and two doses at 2 mg/kg. Results: The results demonstrated that compared of untreated IR group to treated IR groups, AT reduced ventricular wall damage area, serum TNF-? (from SS+IR: 287.42±3.95 pg/ml to AT+IR: 231.28±9.16 pg/ml and AT+I+AT+R : 195.86±13.18 pg/ml, and the level of malondialdehyde (MDA) (MDA = SS+IR: 7.96±0.15 pmol/mg to AT+IR: 5.6±0.14 pmol/mg and AT+I+AT+R: 4.9±0.07 pmol/mg), data expressed in mean ± M. Conclusion: Our research suggested that atenolol reduced cardiac effects against intestinal IR injury in rats, which may be attributed to attenuating inflammation and oxidative stress and ameliorated cardiac dysfunction.
- ItemSomente MetadadadosTLR4 mRNA Levels as Tools to Estimate Risk for Early Posttransplantation Kidney Graft Dysfunction(Lippincott Williams & Wilkins, 2012-09-27) Andrade-Oliveira, Vinicius [UNIFESP]; Campos, Erika F. [UNIFESP]; Goncalves-Primo, Amador; Grenzi, Patricia C. [UNIFESP]; Medina-Pestana, Jose O. [UNIFESP]; Tedesco-Silva, Helio; Gerbase-DeLima, Maria [UNIFESP]; Assoc Fundo Incent Pesquisa; Universidade Federal de São Paulo (UNIFESP); Hosp Rim & HipertensaoBackground. the participation of Toll-like receptor (TLR) 4, an innate immunity receptor, has been previously demonstrated in the pathogenesis of acute renal injury. We aimed to investigate whether messenger RNA (mRNA) levels of TLR4 and its adapter molecule, myeloid differentiation primary response gene (MYD) 88, are associated with delayed graft function (DGF) and could be used as biomarkers of its occurrence.Methods. TLR4 and MYD88 gene mRNA levels were evaluated with real-time polymerase chain reaction, in preimplantation biopsies (n=89) and first day posttransplantation samples of urine (n=67) and blood (n=80) from graft recipients and analyzed according to donor type (living or deceased) and DGF occurrence.Results. Expression levels of both genes were higher in biopsies from deceased donors than from living donors (P<0.001 for both) but did not differ between deceased-donor kidney transplants with and without DGF; in urine, TLR4 expression levels were higher in patients with prolonged DGF (DGF lasting 914 days) (P=0.05, compared with cases without DGF); in blood, lower mRNA levels of TLR4 and MYD88 predicted pDGF occurrence with an accuracy of 86% and 87%, respectively.Conclusion. the expression levels of TLR4 and MYD88 were higher in kidneys from deceased donors than from living donors. Lower levels of expression of both genes in blood were associated with DGF occurrence. the prediction of prolonged DGF by low TLR4 and MYD88 expression levels in blood with a greater the 85% accuracy was the most important finding of this study.