THAIS MARTINS DE LIMA

(Fonte: Lattes)
Índice h a partir de 2011
15
Projetos de Pesquisa
Unidades Organizacionais
LIM/51 - Laboratório de Emergências Clínicas, Hospital das Clínicas, Faculdade de Medicina
LIM/02 - Laboratório de Anatomia Médico-Cirúrgica, Hospital das Clínicas, Faculdade de Medicina

Resultados de Busca

Agora exibindo 1 - 5 de 5
  • article 3 Citação(ões) na Scopus
    Crotoxin modulates inflammation and macrophages? functions in a murine sepsis model
    (2022) BRETONES, Marisa Langeani; SAMPAIO, Sandra Coccuzzo; BARBEIRO, Denise Frediani; ARIGA, Suely K. Kubo; SORIANO, Francisco Garcia; LIMA, Thais Martins de
    Sepsis is a syndrome of physiological and biochemical abnormalities induced by an infection that represents a major public health concern. It involves the early activation of inflammatory responses. Crotoxin (CTX), the major toxin of the South American rattlesnake Crotalus durissus terrificus venom, presents longstanding antiinflammatory properties. Since immune system modulation may be a strategic target in sepsis management, and macrophages' functional and secretory activities are related to the disease's progression, we evaluated the effects of CTX on macrophages from septic animals. Balb/c male mice submitted to cecal ligation and puncture (CLP) were treated with CTX (0.9 mu g/animal, subcutaneously) 1 h after the procedure and euthanized after 6 h. We used plasma samples to quantify circulating cytokines and eicosanoids. Bone marrow differentiated macrophages (BMDM) were used to evaluate the CTX effect on macrophages' functions. Our data show that CTX administration increased the survival rate of the animals from 40% to 80%. Septic mice presented lower plasma concentrations of IL-6 and TNF-alpha after CTX treatment, and higher concentrations of LXA4, PGE2, and IL-1 beta. No effect was observed in IL-10, IFN-gamma, and RD1 concentrations. BMDM from septic mice treated with CTX presented decreased capacity of E. coli phagocytosis, but sustained NO and H2O2 production. We also observed higher IL-6 concentration in the culture medium of BMDM from septic mice, and CTX induced a significant reduction. CTX treatment increased IL-10 production by macrophages as well. Our data show that the protective effect of CTX in sepsis mortality involves modulation of macrophage functions and inflammatory mediators' production.
  • article 2 Citação(ões) na Scopus
    Banana green peels extract protects against nonalcoholic fatty liver disease in high-fat-fed mice through modulation of lipid metabolism and inflammation
    (2022) BARROSO, Wermerson Assuncao; SERRA, Mariana Barreto; ABREU, Iracelle Carvalho; BARBEIRO, Hermes Vieira; FIAMONCINI, Jarlei; ALVARENGA, Jose Fernando Rinaldi de; SOUZA, Heraldo Possolo de; LIMA, Thais Martins de
    We investigate the effect of the banana green peels extract (BPE) as a preventive treatment against NAFLD in high-fat diet fed mice. Mice received daily doses of 100 or 250 mg/kg of BPE for 12 weeks along with the high-fat diet. BPE reduced weight gain (p < .0001), adipose tissue hypertrophy (p < .0001), and improved glucose homeostasis (p < .0001). Plasma levels of glucose-dependent insulinotropic polypeptide, triglycerides, total cholesterol, LDL-cholesterol, non-esterified fatty acids, aspartate and alanine transaminase, leptin, and resistin were decreased in BPE treated mice (p < .05). BPE effects on lipid metabolism were associated with decreased gene expression of lipogenic enzymes and increased expression of enzymes related to fatty acid and cholesterol degradation (p < .05). Plasma and liver bile acid (BA) profiles were modulated by BPE, with positive correlations between specific BA and UCP-1, CPT-1 and PGC-1 beta expression in brown adipose tissue (p < .05). BPE reduced hepatic steatosis and inflammation, possibly due to reduced p65 NF-kappa B nuclear translocation (p < .05) and modulation of oxidative stress (p < .05). These data indicate that BPE is a source of phytochemical compounds with promising effects toward the prevention of metabolic disorders associated with obesity.
  • article 1 Citação(ões) na Scopus
    Short-term Obesity Worsens Heart Inflammation and Disrupts Mitochondrial Biogenesis and Function in an Experimental Model of Endotoxemia
    (2022) PETRONI, Ricardo Costa; OLIVEIRA, Suelen Jeronymo Souza de; FUNGARO, Thais Pineda; ARIGA, Suely K. K.; BARBEIRO, Hermes Vieira; SORIANO, Francisco Garcia; LIMA, Thais Martins de
    Cardiomyopathy is a well-known complication of sepsis that may deteriorate when accompanied by obesity. To test this hypothesis we fed C57black/6 male mice for 6 week with a high fat diet (60% energy) and submitted them to endotoxemic shock using E. coli LPS (10 mg/kg). Inflammatory markers (cytokines and adhesion molecules) were determined in plasma and heart tissue, as well as heart mitochondrial biogenesis and function. Obesity markedly shortened the survival rate of mouse after LPS injection and induced a persistent systemic inflammation since TNF alpha, IL-1 beta, IL-6 and resistin plasma levels were higher 24 h after LPS injection. Heart tissue inflammation was significantly higher in obese mice, as detected by elevated mRNA expression of pro-inflammatory cytokines (IL-1 beta, IL-6 and TNF alpha). Obese animals presented reduced maximum respiratory rate after LPS injection, however fatty acid oxidation increased in both groups. LPS decreased mitochondrial DNA content and mitochondria biogenesis factors, such as PGC1 alpha and PGC1 beta, in both groups, while NRF1 expression was significantly stimulated in obese mice hearts. Mitochondrial fusion/fission balance was only altered by obesity, with no influence of endotoxemia. Obesity accelerated endotoxemia death rate due to higher systemic inflammation and decreased heart mitochondrial respiratory capacity.
  • article 6 Citação(ões) na Scopus
    Endothelial injury in COVID-19 and septic patients
    (2022) HOKAMA, Larissa Tami; VEIGA, Alicia Dudy Muller; MENEZES, Maria Clara Saad; PINTO, Agnes Araujo Sardinha; LIMA, Thais Martins de; ARIGA, Suely Kunimi Kubo; BARBEIRO, Hermes Vieira; BARBEIRO, Denise Frediani; MOREIRA, Claudia de Lucena; STANZANI, Gabriela; BRANDAO, Rodrigo Antonio; MARCHINI, Julio Flavio; ALENCAR, Julio Cesar; MARINO, Lucas Oliveira; GOMEZ, Luz Marina; SOUZA, Heraldo P.
    Systemic inflammatory response, as observed in sepsis and severe COVID-19, may lead to endothelial damage. Therefore, we aim to compare the extent of endothelial injury and its relationship to inflammation in both diseases. We included patients diagnosed with sepsis (SEPSIS group, n = 21), mild COVID-19 (MILD group, n = 31), and severe COVID-19 (SEVERE group, n = 24). Clinical and routine laboratory data were obtained, circulating cytokines (INF-gamma, TNF-alpha, and IL-10) and endothelial injury markers (E-Selectin, Tissue Factor (TF) and von Willebrand factor (vWF)) were measured. Compared to the SEPSIS group, patients with severe COVID-19 present similar clinical and laboratory data, except for lower circulating IL-10 and E-Selectin levels. Compared to the MILD group, patients in the SEVERE group showed higher levels of TNF-alpha, IL-10, and TF. There was no clear relationship between cytokines and endothelial injury markers among the three studied groups; however, in SEVERE COVID-19 patients, there is a positive relationship between INF-gamma with TF and a negative relationship between IL-10 and vWF. In conclusion, COVID-19 and septic patients have a similar pattern of cytokines and endothelial dysfunction markers. These findings highlight the importance of endothelium dysfunction in COVID-19 and suggest that endothelium should be better evaluated as a therapeutic target for the disease.
  • article 5 Citação(ões) na Scopus
    Poor prognosis indicators of type-2 diabetic COVID-19 patients
    (2022) GORJAO, R.; HIRABARA, S. M.; MASI, L. N.; SERDAN, T. D. A.; GRITTE, R. B.; HATANAKA, E.; SOUZA-SIQUEIRA, T.; PITHON-CURI, A. C.; LIMA, T. M. de; PITHON-CURI, T. C.; MARCHINI, J. F. M.; MACHADO, M. C. C.; SOUZA, H. P.; CURI, R.
    Diabetes is associated with a worse prognosis and a high risk of morbidity and mortality in COVID-19 patients. We aimed to evaluate the main factors involved in the poor prognosis in diabetic patients. A total of 984 patients diagnosed with COVID-19 admitted to the hospital were included in this study. Patients were first divided into type-2 diabetic (DM + ) and non-diabetic (DM-) groups. The participants were analyzed based on the National Early Warning Score (NEWS) and on the Quick-Sequential Organ Failure Assessment (qSOFA) to find the best prognostic risk score for our study. The DM + and DM- groups were divided into non-severe and severe groups. Comparative and correlative analyses were used to identify the physiological parameters that could be employed for creating a potential risk indicator for DM + COVID-19 patients. We found a poorer prognosis for the DM + COVID-19 patients with a higher ICU admission rate, mechanical ventilation rate, vasopressor use, dialysis, and longer treatment times compared with the DM- group. DM + COVID-19 patients had increased plasma glucose, lactate, age, urea, NEWS, and D-dimer levels, herein referred to as the GLAUND set, and worse prognosis and outcomes when compared with infected DM- patients. The NEWS score was a better indicator for assessing COVID-19 severity in diabetic patients than the q-SOFA score. In conclusion, diabetic COVID-19 patients should be assessed with the NEWS score and GLAUND set for determining their prognosis COVID-19 prognosis.