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Pesquisa : D08.811.399.475 [Categoria DeCS]
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Id: biblio-1040245
Autor: Khalilpour, Jamal; Roshan-Milani, Shiva; Gharalari, Farzaneh Hosseini; Fard, Amin Abdollahzade.
Título: Macrophage migration inhibitory factor antagonist (p425) ameliorates kidney histopathological and functional changes in diabetic rats / Antagonista (p425) do fator de inibição da migração de macrófagos (MIF) melhora as alterações histopatológicas e funcionais renais em ratos diabéticos
Fonte: J. bras. nefrol;41(3):315-322, July-Sept. 2019. tab, graf.
Idioma: en.
Projeto: Urmia University of Medical Sciences.
Resumo: Abstract Introduction: It is hypothesized that increased macrophage migration inhibitory factor (MIF) expression may contribute to diabetic nephropathy (DN) pathogenesis. The aim of the present study was to investigate the renal effects of MIF inhibition in a diabetic experimental model. Methods: Eighteen male Wistar rats (230 ± 20 g) were divided into three groups: 1) control, 2) diabetic (STZ, 50 mg/kg, dissolved in saline, ip), 3) diabetic + MIF antagonist (p425, 1 mg/kg per day, ip, on the 21th day, for 21 consecutive days). The treatment started since we founwd a significant increase in urine albumin excretion (UAE) rate in the diabetic rats in comparison with the control rats. The rats were kept individually in metabolic cages (8 AM-2 PM) and urine samples were collected in the 21 and 42th day. At the end, blood and tissue samples were collected for biochemical (BS, UPE, urine GAG, BUN, Cr, Na, and K) and histological analyses. Results: The results of this study showed that MIF antagonist (p425) significantly decreased urine protein and GAG excretion, urine protein/creatinine ratio, and serum BUN and Cr in the streptozotocin-induced DN in the rats. Pathological changes were significantly alleviated in the MIF antagonist (p425)-administered DN rats. Conclusion: Collectively, these data suggested that MIF antagonist (p425) was able to protect against functional and histopathological injury in the DN.

Resumo Introdução: Supõe-se que elevações da expressão do fator de inibição da migração de macrófagos (MIF) possam contribuir para a patogênese da nefropatia diabética (ND). O objetivo do presente estudo foi investigar os efeitos renais da inibição do MIF em um modelo experimental diabético. Métodos: Dezoito ratos Wistar machos (230 ± 20g) foram divididos em três grupos: 1) controle, 2) diabético (STZ 50 mg/kg dissolvida em soro fisiológico, IP), 3) diabético + antagonista do MIF (p425 1 mg/kg por dia IP no 21o dia por 21 dias consecutivos). O tratamento começou após a identificação de aumento significativo na albuminúria nos ratos diabéticos em relação aos controles. Os ratos foram mantidos individualmente em gaiolas metabólicas (8h-14h) e amostras de urina foram colhidas no 21o e no 42o dia. Ao final do estudo, amostras de sangue e tecido foram colhidas para análises bioquímicas (BS, excreção urinária de proteína, excreção urinária de GAGs, BUN, Cr, Na e K) e histológicas. Resultados: O presente estudo demonstrou que o antagonista do MIF (p425) diminuiu significativamente proteinúria, excreção urinária de GAGs , relação proteína/creatinina na urina, BUN e Cr no grupo com ND induzida por estreptozotocina. As alterações patológicas foram significativamente abrandadas nos ratos com ND que receberam antagonista do MIF (p425). Conclusão: Coletivamente, os dados sugerem que o antagonista do MIF (p425) teve efeito protetor contra lesões funcionais e histopatológicas da ND.
Descritores: Fatores Inibidores da Migração de Macrófagos/antagonistas & inibidores
Oxirredutases Intramoleculares/antagonistas & inibidores
Substâncias Protetoras/uso terapêutico
Substâncias Protetoras/farmacologia
Diabetes Mellitus Experimental/patologia
Nefropatias Diabéticas/terapia
-Glicemia
Ratos Wistar
Estreptozocina/farmacologia
Creatinina/urina
Creatinina/sangue
Diabetes Mellitus Experimental/induzido quimicamente
Diabetes Mellitus Experimental/urina
Diabetes Mellitus Experimental/sangue
Nefropatias Diabéticas/urina
Nefropatias Diabéticas/patologia
Nefropatias Diabéticas/sangue
Albuminúria/tratamento farmacológico
Modelos Animais de Doenças
Glicosaminoglicanos/urina
Rim/patologia
Ativação de Macrófagos
Limites: Animais
Masculino
Ratos
Responsável: BR1.1 - BIREME


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Id: lil-686569
Autor: Rao, F.; Deng, C.Y.; Zhang, Q.H.; Xue, Y.M.; Xiao, D.Z.; Kuang, S.J.; Lin, Q.X.; Shan, Z.X.; Liu, X.Y.; Zhu, J.N.; Yu, X.Y.; Wu, S.L..
Título: Involvement of Src tyrosine kinase and protein kinase C in the expression of macrophage migration inhibitory factor induced by H2O2 in HL-1 mouse cardiac muscle cells
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;46(9):746-751, 19/set. 2013. graf.
Idioma: en.
Projeto: the National Natural Science Foundation of China; . the National Natural Science Foundation of China; . the China Postdoctoral Science Foundation; . the Guangdong Provincial Natural Science Foundation; . the Guangdong Provincial Natural Science Foundation; . the Medical Scientific Research Foundation of Guangdong Province; . the Medical Scientific Research Foundation of Guangdong Province.
Resumo: Macrophage migration inhibitory factor (MIF), a pleiotropic cytokine, plays an important role in the pathogenesis of atrial fibrillation; however, the upstream regulation of MIF in atrial myocytes remains unclear. In the present study, we investigated whether and how MIF is regulated in response to the renin-angiotensin system and oxidative stress in atrium myocytes (HL-1 cells). MIF protein and mRNA levels in HL-1 cells were assayed using immunofluorescence, real-time PCR, and Western blot. The result indicated that MIF was expressed in the cytoplasm of HL-1 cells. Hydrogen peroxide (H2O2), but not angiotensin II, stimulated MIF expression in HL-1 cells. H2O2-induced MIF protein and gene levels increased in a dose-dependent manner and were completely abolished in the presence of catalase. H2O2-induced MIF production was completely inhibited by tyrosine kinase inhibitors genistein and PP1, as well as by protein kinase C (PKC) inhibitor GF109203X, suggesting that redox-sensitive MIF production is mediated through tyrosine kinase and PKC-dependent mechanisms in HL-1 cells. These results suggest that MIF is upregulated by HL-1 cells in response to redox stress, probably by the activation of Src and PKC.
Descritores: Peróxido de Hidrogênio/farmacologia
Oxirredutases Intramoleculares/efeitos dos fármacos
Fatores Inibidores da Migração de Macrófagos/efeitos dos fármacos
Miócitos Cardíacos/metabolismo
Oxidantes/farmacologia
Proteína Quinase C/metabolismo
Quinases da Família src/metabolismo
-Angiotensina II/metabolismo
Western Blotting
Linhagem Celular
Imuno-Histoquímica
Oxirredutases Intramoleculares/genética
Microscopia Confocal
Fatores Inibidores da Migração de Macrófagos/genética
Estresse Oxidativo/fisiologia
Inibidores de Proteínas Quinases/farmacologia
Reação em Cadeia da Polimerase em Tempo Real
Sistema Renina-Angiotensina/fisiologia
Limites: Animais
Camundongos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


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Id: lil-595040
Autor: Denninghoff, Valeria C; Ossani, Georgina P; Uceda, Ana M; Avagnina, Maria A; Elsner, Boris; Monserrat, Alberto J.
Título: Variable number tandem repeats in the promoter region of prostacyclin synthase gene in choline deficient rats
Fonte: Biocell;34(2):65-70, Aug. 2010. tab.
Idioma: en.
Resumo: Weanling Sprague-Dawley rats were fed on a choline-deficient diet with hydrogenated vegetable oil and corn oil as lipids develop acute renal failure. Pathogenesis of the latter is controversial and an ischemic mechanism has been proposed. Arachidonic acid derivatives are involved in the regulation of vascular tonus. Vasospasm could be due to an increase in tromboxane A2-mediated vasoconstriction or to a decrease in prostacyclin-induced vasodilatation. Enzymes involved in the synthesis of both compounds are tromboxane A2- and prostacyclin-synthase respectively. The aim of this study was to identify the variable number tandem repeats (VNTR) in the promoter region of prostacyclin synthase gene and verify if there exists a relationship between the occurrence of VNTR in those choline-deficient rats which die because of acute renal failure and those which do not. We verified the presence of the VNTR in the prostacyclin synthase rat gene, but we did not find any difference in the molecular weight of the alleles between experimental and control rats. Renal reparation of the acute kidney injury due to choline deficiency in some rats is not related with differences in VNTR in the promoter region of the prostacyclin synthase gene.
Descritores: Deficiência de Colina/genética
Oxirredutases Intramoleculares/genética
/genética
SISTEMA ENZIMATICO DEL CITOCROMO P-ALDEHYDES/genética
-Dieta
Repetições Minissatélites
Ratos Sprague-Dawley
Limites: Humanos
Masculino
Animais
Feminino
Gravidez
Ratos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: AR40.1 - Biblioteca de la Facultad de Ciencias Médicas de la UNCuyo



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