ELIA TAMASO ESPIN GARCIA CALZOLARI
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Patologia, Faculdade de Medicina - Docente
LIM/59 - Laboratório de Biologia Celular, Hospital das Clínicas, Faculdade de Medicina
LIM/59 - Laboratório de Biologia Celular, Hospital das Clínicas, Faculdade de Medicina
7 resultados
Resultados de Busca
Agora exibindo 1 - 7 de 7
- Baroreflex Impairment Precedes Cardiometabolic Dysfunction in an Experimental Model of Metabolic Syndrome: Role of Inflammation and Oxidative Stress(2018) BERNARDES, Nathalia; DIAS, Danielle da Silva; STOYELL-CONTI, Filipe Fernandes; BRITO-MONZANI, Janaina de Oliveira; MALFITANO, Christiane; CALDINI, Elia Garcia; ULLOA, Luis; LLESUY, Susana Francisca; IRIGOYEN, Maria-Claudia; ANGELIS, Katia DeThis study analyzes whether autonomic dysfunction precedes cardiometabolic alterations in spontaneously hypertensive rats (SHR) with fructose overload. Animals were randomly distributed into three groups: control, hypertensive and hypertensive with fructose overload. Fructose overload (100 g/L) was initiated at 30 days old, and the animals (n = 6/group/time) were evaluated after 7,15, 30 and 60 days of fructose consumption. Fructose consumption reduced baroreflex sensitivity by day 7, and still induced a progressive reduction in baroreflex sensitivity over the time. Fructose consumption also increased TNF alpha and IL-6 levels in the adipose tissue and IL-1 beta(3 levels in the spleen at days 15 and 30. Fructose consumption also reduced plasmatic nitrites (day 15 and 30) and superoxide dismutase activity (day 15 and 60), but increased hydrogen peroxide (day 30 and 60), lipid peroxidation and protein oxidation (day 60). Fructose consumption increased arterial pressure at day 30 (8%) and 60 (11%). Fructose consumption also induced a late insulin resistance at day 60, but did not affect glucose levels. In conclusion, the results show that baroreflex sensitivity impairment precedes inflammatory and oxidative stress disorders, probably by inducing hemodynamic and metabolic dysfunctions observed in metabolic syndrome.
- Aerobic exercise inhibits obesity-induced respiratory phenotype(2018) AQUINO-JUNIOR, Jefferson Comin Jonco; MACKENZIE, BreAnne; ALMEIDA-OLIVEIRA, Ana Roberta; MARTINS, Ana Carolina; OLIVEIRA-JUNIOR, Manoel Carneiro; BRITTO, Aurilea Aparecida; ARANTES-COSTA, Fernanda Magalhaes; DAMACENO-RODRIGUES, Nilsa Regina; CALDINI, Elia Garcia; OLIVEIRA, Ana Paula Ligeiro de; GUADAGNINI, Dioze; LEIRIA, Luiz Osorio; RICARDO, Djalma Rabelo; SAAD, Mario Jose Abdalla; VIEIRA, Rodolfo PaulaPurpose: Obesity results in decreased lung function and increased inflammation. Moderate aerobic exercise (AE) reduced lung inflammation and remodeling in a variety of respiratory disease models. Therefore, this study investigated whether AE can attenuate a diet-induced obesity respiratory phenotype; including airway hyperresponsiveness (AHR), remodeling and inflammation.& para;& para;Methods: Sixty C57B1/6 male mice were distributed into four groups: control lean (CL), exercise lean (EL), obese (O) and obese exercise (OE) groups (2 sets of 7 and 8 mice per group; n = 15). A classical model of diet-induced obesity (DIO) over 12 weeks was used. AE was performed 60 min/day, 5 days/week for 5 weeks. Airway hyperresponsiveness (AHR), lung inflammation and remodeling, adipokines and cytokines in bronchoalveolar lavage (BAL) was determined.& para;& para;Results: A high fat diet over 18 weeks significantly increased body weight (p < .0001). Five weeks of AE significantly reduced both AHR and pulmonary inflammation. AHR in obese mice that exercised was reduced at the basal level (p < .05), vehicle (PBS) (p < .05), 6.25 MCh mg/mL (p < .05), 12.5 MCh mg/mL (p < .01), 25 MCh mg/mL (p < .01) and 50 MCh mg/mL (p < .05). Collagen (p < .001) and elastic (p < .001) fiber deposition in airway wall and also smooth muscle thickness (p < .001) were reduced. The number of neutrophils (p < .001), macrophages (p < .001) and lymphocytes (p < .01) were reduced in the peribronchial space as well as in the BAL: lymphocytes (p < .01), macrophages (p < .01), neutrophils (p < .001). AE reduced obesity markers leptin (p < .001), IGF-1 (p < .01) and VEGF (p < .001), while increased adiponectin (p < .01) in BAL. AE also reduced pro-inflammatory cytokines in the SAL: IL-1 beta (p < .001), IL-12p40 (p < .001), IL-13 (p < .01), IL-17 (p < .001, IL-23 (p < .05) and TNF-alpha (p < .05), and increased antiinflammatory cytokine IL-10 (p < .05).& para;& para;Conclusions: Aerobic exercise reduces high fat diet-induced obese lung phenotype (AHR, pulmonary remodeling and inflammation), involving anti-inflammatory cytokine IL-10 and adiponectin.
- EFFECT OF SUPPLEMENTATION OF FRUIT EXTRACT (CRANBERRRY, BLUEBERRY AND POMEGRANATE) ON INSULIN RESISTANCE AND OXIDATIVE STRESS IN HYPERTENSIVE PATIENTS(2018) GAETA, L. N. N.; MORAES, M. C.; KATAYAMA, K. Y.; SANGALETTI, C. T.; IRIGOYEN, M. C.; FREITAS, S.; VIANA, A.; ANGELIS, K. De; LOPES, H. F.; CALDINI, Elia C.
- Aerobic Exercise Protects from Pseudomonas aeruginosa-Induced Pneumonia in Elderly Mice(2018) DURIGON, Thomas Stravinskas; MACKENZIE, BreAnne; OLIVEIRA-JUNIOR, Manoel Carneiro; SANTOS-DIAS, Alana; ANGELIS, Katia De; MALFITANO, Christiano; PALMA, Renata Kelly da; GUERRA, Juliana Moreno; DAMACENO-RODRIGUES, Nilsa Regina; CALDINI, Elia Garcia; ALMEIDA, Francine Maria de; AQUINO-SANTOS, Helida Cristina; RIGONATO-OLIVEIRA, Nicole Cristine; OLIVEIRA, Danielle Bruna Leal de; AIMBIRE, Flavio; OLIVEIRA, Ana Paula Ligeiro de; OLIVEIRA, Luiz Vicente Franco de; DURIGON, Edison Luiz; HIEMSTRA, Pieter S.; VIEIRA, Rodolfo P.Background: Pseudomonas aeruginosa (PS) infection results in severe morbidity and mortality, especially in immune-deficient populations. Aerobic exercise (AE) modulates the immune system, but its effects on the outcomes of pulmonary PS infection in elderly mice are unknown. Methods: BALB/c mice (24 weeks old) were randomized to sedentary, exercise (EX), PS, and PS + EX groups for the acute experimental setting, and PS and PS + EX groups for the chronic setting. Low-intensity AE was performed for 5 weeks, 60 min/day; 24 h after the final AE session, mice were inoculated with 5 x 10(4) colony-forming units (CFU) of PS, and 24 h and 14 days after PS inoculation, mice were studied. Results: AE inhibited PS colonization (p < 0.001) and lung inflammation (total cells, neutrophils, lymphocytes [p < 0.01] in bronchoalveolar lavage [BAL]), with significant differences in BAL levels of IL-1 beta (p < 0.001), IL-6 (p < 0.01), CXCL1 (p < 0.001), and TNF-alpha (p < 0.001), as well as parenchymal neutrophils (p < 0.001). AE increased BAL levels of IL-10 and parenchymal (p < 0.001) and epithelial (p < 0.001) IL-10 expression, while epithelial (p < 0.001) and parenchymal (p < 0.001) NF-kappa B expression was decreased. AE diminished pulmonary lipid peroxidation (p < 0.001) and increased glutathione peroxidase (p < 0.01). Preincubation of BEAS-2B with IL-10 inhibited PS-induced epithelial cell expression of TNF-alpha (p < 0.05), CD40 (p < 0.01), and dichlorodihydrofluorescein diacetate (p < 0.05). Conclusions: AE inhibits PS-induced lung inflammation and bacterial colonization in elderly mice, involving IL-10/ NF-.B, and redox signaling. (C) 2018 S. Karger AG, Basel
- Blockade of AT1 type receptors for angiotensin II prevents cardiac microvascular fibrosis induced by chronic stress in Sprague-Dawley rats(2018) FIROOZMAND, Lilia Taddeo; SANCHES, Andrea; DAMACENO-RODRIGUES, Nilsa Regina; PEREZ, Juliana Dineia; ARAGAO, Danielle Sanches; ROSA, Rodolfo Mattar; MARCONDES, Fernanda Klein; CASARINI, Dulce Elena; CALDINI, Elia Garcia; CUNHA, Tatiana SousaTo test the effects of chronic-stress on the cardiovascular system, the model of chronic mild unpredictable stress (CMS) has been widely used. The CMS protocol consists of the random, intermittent, and unpredictable exposure of laboratory animals to a variety of stressors, during 3 consecutive weeks. In this study, we tested the hypothesis that exposure to the CMS protocol leads to left ventricle microcirculatory remodeling that can be attenuated by angiotensin II receptor blockade. Male Sprague-Dawley rats were randomly assigned into four groups: Control, Stress, Control + losartan, and Stress + losartan (N = 6, each group, losartan: 20 mg/kg/day). The rats were euthanized 15 days after CMS exposure, and blood samples and left ventricle were collected. Rats submitted to CMS presented increased glycemia, corticosterone, noradrenaline and adrenaline concentration, and losartan reduced the concentration of the circulating amines. Cardiac angiotensin II, measured by high-performance liquid chromatography (HPLC), was significantly increased in the CMS group, and losartan treatment reduced it, while angiotensin 1-7 was significantly higher in the CMS losartan-treated group as compared with CMS. Histological analysis, verified by transmission electron microscopy, showed that rats exposed to CMS presented increased perivascular collagen and losartan effectively prevented the development of this process. Hence, CMS induced a state of microvascular disease, with increased perivascular collagen deposition, that may be the trigger for further development of cardiovascular disease. In this case, CMS fibrosis is associated with increased production of catecholamines and with a disruption of renin-angiotensin system balance, which can be prevented by angiotensin II receptor blockade.
- Acute acalculous cholecystitis during zika virus infection in an immunocompromised patient(2018) ONO, Suzane Kioko; BASSIT, Leda; VAISBERG, Victor Van; ALVES, Venancio Avancini Ferreira; CALDINI, Elia G.; HERMAN, Brian D.; SHABMAN, Reed; FEDOROVA, Nadia B.; PARANAGUA-VEZOZZO, Denise; SAMPAIO, Caroline Torres; LAGES, Rafael Bandeira; TERRABUIO, Debora; ANDRAUS, Wellington; SCHINAZI, Raymond F.; CARRILHO, Flair Jose
- Cell internalization of 7-ketocholesterol-containing nanoemulsion through LDL receptor reduces melanoma growth in vitro and in vivo: A preliminary report(2018) FAVERO, G. M.; PAZ, J. L.; OTAKE, A. H.; MARIA, D. A.; CALDINI, E. G.; MEDEIROS, R. S. S. de; DEUS, D. F.; CHAMMAS, R.; MARANHãO, R. C.; BYDLOWSKI, S. P.Oxysterols are cholesterol oxygenated derivatives which possess several biological actions. Among oxysterols, 7-ketocholesterol (7KC) is known to induce cell death. Here, we hypothesized that 7KC cytotoxicity could be applied in cancer therapeutics. 7KC was incorporated into a lipid core nanoemulsion. As a cellular model the murine melanoma cell line B16F10 was used. The nanoparticle (7KCLDE) uptake into tumor cells was displaced by increasing amounts of low-density-lipoproteins (LDL) suggesting a LDL-receptor-mediated cell internalization. 7KCLDE was mainly cytostatic, which led to an accumulation of polyploid cells. Nevertheless, a single dose of 7KCLDE killed roughly 10% of melanoma cells. In addition, it was observed dissipation of the transmembrane potential, evidenced with flow cytometry; presence of autophagic vacuoles, visualized and quantified with flow cytometry and acridine orange; and presence of myelin figures, observed with ultrastructural microscopy. 7KCLDE impaired cytokenesis was accompanied by changes in cellular morphology into a fibroblastoid shape which is supported by cytoskeletal rearrangements, as shown by the increased actin polymerization. 7KCLDE was injected into B16 melanoma tumor-bearing mice. 7KCLDE accumulated in the liver and tumor. In melanoma tumor 7KCLDE promoted a > 50% size reduction, enlarged the necrotic area, and reduced intratumoral vasculature. 7KCLDE increased the survival rates of animals, without hematologic or liver toxicity. Although more pre-clinical studies should be performed, our preliminary results suggested that 7KCLDE is a promising novel preparation for cancer chemotherapy. © Favero et al.