RICARDO COSTA PETRONI
Projetos de Pesquisa
Unidades Organizacionais
LIM/51 - Laboratório de Emergências Clínicas, Hospital das Clínicas, Faculdade de Medicina
5 resultados
Resultados de Busca
Agora exibindo 1 - 5 de 5
- High-fat diet inhibits PGC-1 alpha suppressive effect on NF kappa B signaling in hepatocytes(2018) BARROSO, Wermerson Assuncao; VICTORINO, Vanessa Jacob; JEREMIAS, Isabela Casagrande; PETRONI, Ricardo Costa; ARIGA, Suely Kunimi Kubo; SALLES, Thiago A.; BARBEIRO, Denise Frediani; LIMA, Thais Martins de; SOUZA, Heraldo Possolo deThe peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1 alpha) regulates the expression of genes implicated in fatty acid oxidation and oxidative phosphorylation. Its role in liver steatosis is well established, since mice with liver-specific deletion of PGC-1 alpha exhibit lipid accumulation and high-fat diet reduces hepatic PGC-1 alpha expression in mice. In this study, we investigated the role of PGC-1 alpha in the inflammatory changes observed in steatohepatitis induced by high-fat diet. C57black/6 mice were fed a high-fat diet containing 30% fat for 10 weeks. After euthanasia, liver morphology was examined by HE staining and inflammation was determined by IL-6, TNF-alpha, and IL-1 beta quantification. Liver gene expression of PGC-1 isoforms was evaluated by real-time PCR and p65 NF kappa B nuclear translocation by Western blotting. HepG2 cells were treated with linoleic acid overload for 72 h to create an in vitro model of steatohepatitis. RNA interference (RNAi) was used to evaluate the involvement of PGC-1 alpha on inflammatory mediators' production by hepatocytes. The high-fat diet led to a state of nonalcoholic steatohepatitis, associated with increased deposits of intra-abdominal fat, hyperglycemia and hyperlipidemia. Mice liver also exhibited increased proinflammatory cytokines' levels, decreased PGC-1 alpha expression, and marked increase in p65 NF kappa B nuclear translocation. Linoleic acid treated cells also presented increased expression of proinflammatory cytokines and decreased PGC-1 alpha expression. The knockdown of PGC-1 alpha content caused an increase in IL-6 expression and release via enhanced I kappa B alpha phosphorylation and subsequent increase of p65 NF kappa B nuclear translocation. High-fat diet induces liver inflammation by inhibiting PGC-1 alpha expression and its suppressive effect in NF kappa B pathway.
conferenceObject Obesity protects heart but increases lung injury by endotoxin inflammation(2014) LIMA, T. M. D.; MALDONADO, M. C.; PETRONI, R.; BARBEIRO, D.; SORIANO, F. G.; SILVA, F. Pinheiro da- Hypertonic saline solution reduces the inflammatory response in endotoxemic rats(2012) THEOBALDO, Mariana Cardillo; BARBEIRO, Hermes Vieira; BARBEIRO, Denise Frediani; PETRONI, Ricardo; SORIANO, Francisco GarciaOBJECTIVE: Volume replacement in septic patients improves hemodynamic stability. This effect can reduce the inflammatory response. The objective of this study was to evaluate the effect of 7.5% hypertonic saline solution versus 0.9% normal saline solution for volume replacement during an inflammatory response in endotoxemic rats. METHODS: We measured cytokines (serum and gut), nitrite, and lipid peroxidation (TBARS) as indicators of oxidative stress in the gut. Rats were divided into four groups: control group (C) that did not receive lipopolysaccharide; lipopolysaccharide injection without treatment (LPS); lipopolysaccharide injection with saline treatment (LPS + S); and lipopolysaccharide injection with hypertonic saline treatment (LPS + H). Serum and intestine were collected. Measurements were taken at 1.5, 8, and 24 h after lipopolysaccharide administration. RESULTS: Of the four groups, the LPS + H group had the highest survival rate. Hypertonic saline solution treatment led to lower levels of IL-6, IL-10, nitric oxide, and thiobarbituric acid reactive substances compared to 0.9% normal saline. In addition, hypertonic saline treatment resulted in a lower mortality compared to 0.9% normal saline treatment in endotoxemic rats. Volume replacement reduced levels of inflammatory mediators in the plasma and gut. CONCLUSION: Hypertonic saline treatment reduced mortality and lowered levels of inflammatory mediators in endotoxemic rats. Hypertonic saline also has the advantage of requiring less volume replacement.
- Hypertonic solution-induced preconditioning reduces inflammation and mortality rate(2019) PIMENTEL, Rosangela Nascimento; PETRONI, Ricardo Costa; BARBEIRO, Hermes Vieira; BARBEIRO, Denise Frediani; ANDRADE, Mariana Macedo; ARIGA, Suely Kumini; SORIANO, Francisco GarciaBackgroundDysregulated inflammatory response is common cause of organ damage in critical care patients. Preconditioning/tolerance is a strategy to prevent exacerbated inflammation. The aim of this study is to analyze hypertonic saline 7.5% as a potential inducer of preconditioning that protect from a lethal dose of LPS and modulates systemic inflammatory profile in mice.MethodsMale Balb/C mice received intravenous (i.v.) injections of Hypertonic solution (NaCl 7.5%) (0.8ml) for 3days, on day 8th was challenged with LPS 15mg/kg. Controls with Saline 0.9%, urea and sorbitol were performed. Microarray of mRNA expression was analyzed from HS versus saline from macrophages to identified the pathways activated by HS.ResultsHS preconditioning reduced mortality after LPS injection as well reduced the cytokines release in plasma of the animals challenged by LPS. In order to check how HS induces a preconditioning state we measured plasma cytokines after each HS infusion. Repeated HS injections induced a state of preconditioning that reprograms the inflammatory response, resulting in reduced inflammatory cytokine production. A microarray of mRNA demonstrated that Hypertonic solution increased the expression of several genes in special Mapkbp1 and Atf3.Conclusionhypertonic solution induces preconditioning/tolerance reducing mortality and inflammatory response after LPS challenge.
conferenceObject Obesity alters sepsis induced pulmonary inflammation(2012) LIMA-SALGADO, T.; FUNGARO, T. P.; PETRONI, R. C.; OLIVEIRA, S. J. S.; BARBEIRO, D. F.; SORIANO, F. G.Purpose/Objective: Sepsis is a severe disease that represents a significant healthcare burden worldwide, while obesity has reached epidemic proportions over the last few decades. Although the mechanism is uncharted, it is known that obesity increases morbidity and mortality in sepsis through its multiple effects on many organ systems, including pulmonary function. Our aim was to investigate the effects of obesity in systemic and pulmonary inflammatory process in an experimental model of endotoxemic shock. Materials and methods: Animals were fed a high fat diet (30% of fat) for 6 weeks and then injected with 15 mg/kg LPS i.p. They were euthanatized after 6, 24 and 48 h. Inflammation was characterized by measurement of plasma and pulmonary cytokines. The mRN expression of cytokines and tissue remodeling proteins was determined by real time PCR. Results: Obesity decreased the survival rate of the animals 24 h after LPS injection. There was higher plasma concentration of IL1-beta, IL-6and TNF-alpha in these animals. Furthermore, there was higher concentration of IL-6 in the obese mice’s lungs after 6 h of endotoxemia. However, the mRNA expression of pro-inflammatory factors (IL-6, TNF-alpha, IL-1beta and MMP9) was lower, suggesting they may be converted to proteins. Obese mice presented higher mRNA expression of TGF-beta after 6 h, indicating a reparative process. Conclusions: Obesity may be an additional complication factor in sepsis induced pulmonary inflammation.