JACQUELINE DE FATIMA JACYSYN
Projetos de Pesquisa
Unidades Organizacionais
LIM/08 - Laboratório de Anestesiologia, Hospital das Clínicas, Faculdade de Medicina
4 resultados
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- Ischemic preconditioning modifies mortality and inflammatory response(2016) PINHEIRO, Daniel Faria de Campos; FONTES, Belchor; SHIMAZAKI, John Kioshi; HEIMBECKER, Ana Maria Cattani; JACYSYN, Jacqueline de Fatima; RASSLAN, Samir; MONTERO, Edna Frasson de Souza; UTIYAMA, Edivaldo MassazoPURPOSE: To evaluate the effect of ischemic preconditioning on mortality, inflammatory mediators and oxidative stress after intestinal ischemia and reperfusion. METHODS: Male Wistar rats were allocated according to the period of ischemia with or without ischemic preconditioning which consist on clamping the superior mesenteric artery for 10 minutes followed by reperfusion for 10 minutes before the sustained ischemia period. Mortality was assessed in Phase 1 study, and the CINC-1, CINC-2 and MDA levels in the lungs were analyzed in Phase 2. RESULTS: Mortality was lower in the ischemic preconditioning group subjected to 90 minutes of ischemia compared to the group without ischemic preconditioning (I-90: 50% and IPC-90: 15%, p=0.018), and it was lower in the ischemic preconditioning group as a whole compared to the groups without ischemic preconditioning (IPC-14% and I=30%, p=0.006). Lower levels of MDA, CINC-1, and CINC-2 were observed in the animals that were subjected to ischemic preconditioning compared to the animals that were not (MDA: I-45=1.23 nmol/mg protein, and IPC-45=0.62 nmol/mg protein, p=0.0333; CINC-1: I-45=0.82 ng/mL and IPC-45=0.67 ng/mL, p=0.041; CINC-2: I-45=0.52 ng/mL and IPC-45=0.35 ng/mL, p=0.032). CONCLUSION: Ischemic preconditioning reduces mortality, inflammatory process and oxidative stress in rats subjected to intestinal ischemia and reperfusion.
- Cytotoxicity of cashew flavonoids towards malignant cell lines(2012) KONAN, Nzi Andre; LINCOPAN, Nilton; DIAZ, Ingrit Elida Collantes; JACYSYN, Jacqueline de Fatima; TIBA, Mirtes Midori Tanae; MENDES, Joao Gustavo Pessini Amarante; BACCHI, Elfriede Marianne; SPIRA, BenyThe leaves of the Cashew plant (Anacardium occidentale L.) are used by the folk medicine in South America and West Africa. This plant is rich in flavonoids, which are polyphenolic compounds widespread in plants, and that have diverse physiological effects. In a sub-acute toxicity assay it was found that an ethanolic extract of Cashew leaves elicited lymphopenia in rats. The extract was also found to be cytotoxic and to induce apoptosis in Jurkat (acute lymphoblastic leukemia) cells. The crude ethanolic extract was fractionated and resolved by HPLC. One of the four fractions obtained led to the isolation of the biflavonoid agasthisflavone. [H-3]-thymidine incorporation assays and flow cytometry analysis showed that the isolated compound displayed a high anti-proliferative effect in Jurkat cells with an IC50 of 2.4 mu g/ml (4.45 mu M). The effect of agathisflavone on the acute promyelocytic leukemia cell line HL60, Burkitt lymphoma Raji cells and Hep-2 laryngeal carcinoma cells was also tested. The two latter ones were only mildly affected by agathisflavone. It is also shown that agathisflavone induces apoptosis in Jurkat cells and it this proposed that this is the likely mechanism of agathisflavone specific cytotoxicity.
- Immunomodulatory effects of crotoxin isolated from Crotalus durissus terrificus venom in mice immunised with human serum albumin(2011) FAVORETTO, B. C.; RICARDI, R.; SILVA, S. R.; JACYSYN, J. F.; FERNANDES, I.; TAKEHARA, H. A.; FAQUIM-MAURO, E. L.Crotalus durissus terrificus venom and its main component, crotoxin (CTX), have the ability to down-modulate the immune system. Certain mechanisms mediated by cells and soluble factors of the immune system are responsible for the elimination of pathogenic molecules to ensure the specific protection against subsequent antigen contact. Accordingly, we evaluated the immunomodulatory effects of CTX on the immune response of mice that had been previously primed by immunisation with human serum albumin (HSA). CTX inoculation after HSA immunisation, along with complete Freund's adjuvant (CFA) or Aluminium hydroxide (Alum) immunisation, was able to suppress anti-HSA IgG1 and IgG2a antibody production. We showed that the inhibitory effects of this toxin are not mediated by necrosis or apoptosis of any lymphoid cell population. Lower proliferation of T lymphocytes from mice immunised with HSA/CFA or HSA/Alum that received the toxin was observed in comparison to the mice that were only immunised. In conclusion, CTX is able to exert potent inhibitory effects on humoural and cellular responses induced by HSA immunisation, even when injected after an innate immune response has been initiated.
- Evidence of bone marrow downregulation in brain-dead rats(2017) MENEGAT, Laura; SIMAS, Rafael; CALIMAN, Julia M.; ZANONI, Fernando L.; JACYSYN, Jacqueline F.; SILVA, Luiz Fernando F. da; BORELLI, Primavera; MOREIRA, Luiz Felipe P.; SANNOMIYA, PaulinaExperimental findings support the evidence of a persistent leucopenia triggered by brain death (BD). This study aimed to investigate leucocyte behaviour in bone marrow and blood after BD in rats. BD was induced using intracranial balloon catheter inflation. Sham-operated (SH) rats were trepanned only. Thereafter bone marrow cells were harvested every six hours from the femoral cavity and used for total and differential counts. They were analysed further by flow cytometry to characterize lymphocyte subsets, granulocyte adhesion molecules expression and apoptosis/necrosis [ annexin V/propidium iodide (PI) protocol]. BD rats exhibited a reduction in bone marrow cells due to a reduction in lymphocytes (40%) and segmented cells (45%). Bone marrow lymphocyte subsets were similar in BD and SH rats (CD3, P = 0.1; CD4, P = 0.4; CD3/CD4, P = 0.4; CD5, P = 0.4, CD3/CD5, P = 0.2; CD8, P = 0.8). Expression of L-selectin and beta(2)-integrins on granulocytes did not differ (CD11a, P = 0.9; CD11b/c, P = 0.7; CD62L, P = 0.1). There were no differences in the percentage of apoptosis and necrosis (Annexin V, P = 0.73; PI, P = 0.21; Annexin V/PI, P = 0.29). In conclusion, data presented suggest that the downregulation of the bone marrow is triggered by brain death itself, and it is not related to changes in lymphocyte subsets, granulocyte adhesion molecules expression or apoptosis and necrosis.