Assuntos
Infarto Encefálico/complicações , Infarto Encefálico/terapia , Hemorragia Cerebral/complicações , Hemorragia Cerebral/terapia , Medicina Integrativa , Doença Aguda , Idoso , Infarto Encefálico/diagnóstico por imagem , Hemorragia Cerebral/diagnóstico por imagem , Humanos , Angiografia por Ressonância Magnética , Imageamento por Ressonância Magnética , Masculino , Tomografia Computadorizada por Raios XRESUMO
AIM: To investigate if iron deposition and fat accumulation in the liver play a pathogenetic role in dimethylnitrosamine (DMN)-induced liver fibrosis in rat. METHODS: Thirty rats were treated with DMN at does consecutive days of 10 microL/kg daily, i.p., for 3 consecutive day each week for 4 wk. Rats (n=30) were sacrificed on the first day (model group A) and 21(st) d (model group B) after cessation of DMN injection. The control group (n=10) received an equivalent amount of saline. Liver tissues were stained with hematoxylin and eosin (HE) and Masson and Prussian blue assay and observed under electron microscopy. Serum alanine aminotransferase (ALT) and liver tissue hydroxyproline (Hyp) content were tested. RESULTS: The liver fibrosis did not automatically reverse, which was similar to previous reports, the perilobular deposition of iron accompanied with collagen showed marked characteristics at both the first and 21(st) d after cessation of DMN injection. However, fat accumulation in hepatocytes occurred only at the 21(st) d after cessation of DMN injection. CONCLUSION: Iron deposition and fat accumulation may play important roles in pathological changes in DMN-induced rat liver fibrosis. The detailed mechanisms of these characteristics need further research.