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J Immunotoxicol ; 13(3): 393-402, 2016 05.
Artigo em Inglês | MEDLINE | ID: mdl-26606075

RESUMO

The current study investigated the combinatorial effect of pravastatin (PRAV) and bone marrow mononuclear cells (BM-MNC) on acute myocardial infarction (AMI) induced experimentally in rats. After induction of MI, rats were given oral PRAV (20 mg/kg/day) for 28 days or a bolus intravenous injection (via lateral vein) of a total of 14 × 10(6) autologous BM-MNC or a combination of both. Serum brain natriuretic peptide (BNP) and histologic changes in cardiac tissues were assessed. Cardiac contents of lipid peroxides, superoxide dismutase (SOD) and inflammatory biomarkers including tumor necrosis factor (TNF)-α and interleukin (IL)-1ß as well as vascular endothelial growth factor (VEGF) and nitric oxide (NO) were also measured. Combined PRAV and BM-MNC treatment significantly suppressed serum BNP. Cardiac cell apoptosis and inflammatory cell infiltration in heart tissue decreased significantly in both the PRAV and the PRAV + BM-MNC groups. Cardiac lipid peroxides along with TNFα and IL-1ß levels were significantly reduced in both the PRAV and PRAV + BM-MNC hosts with an increase in SOD levels. However, the combined treatment increased cardiac NO levels and did not modify cardiac VEGF levels. The current results indicated that administration of BM-MNC improved the therapeutic efficacy of PRAV treatment by improving the morphology of infarcted hearts as well as decreasing inflammation in a host, but did not do so by inducing therapeutic angiogenesis.


Assuntos
Anti-Inflamatórios/uso terapêutico , Isoproterenol/efeitos adversos , Monócitos/imunologia , Infarto do Miocárdio/imunologia , Miocárdio/patologia , Pravastatina/uso terapêutico , Animais , Apoptose/efeitos dos fármacos , Células da Medula Óssea/imunologia , Terapia Combinada , Citocinas/metabolismo , Humanos , Isoproterenol/administração & dosagem , Peroxidação de Lipídeos/efeitos dos fármacos , Masculino , Modelos Animais , Monócitos/transplante , Infarto do Miocárdio/induzido quimicamente , Infarto do Miocárdio/tratamento farmacológico , Peptídeo Natriurético Encefálico/sangue , Estresse Oxidativo/efeitos dos fármacos , Ratos , Ratos Wistar , Fator A de Crescimento do Endotélio Vascular/metabolismo
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