مرکز منطقه ای اطلاع رساني علوم و فناوري -

چكيده لاتين :

The anti-apoptotic gene bcl-2 is located in mitochondria, but it is uncertain whether its expression affects hepatocyte survival in ischemia/reperfusion (I/R) injury. This experiment was designed to evaluate the role of folic acid in expression of bel2 in IIR in rat liver. Eighteen Wister rats were divided into sham-operated control group (C) (n=6), IJR group (n=6) , folic acid treated group which received I mg/kg/day folic acid by oral route for 7 days before induction of IIR (n=6). Bcl-2 expression was measured by RT-PCR and western blot methods. Folic acid significantly increased Bcl-2 mRNA expression in comparison to the IIR group. Quantification of apoptotic and necrotic hepatocytes, measured by fluorescence microscopy and terminal deoxynucleotidyl transferase (TdT)-mediated dUDPbiotin nick end labeling (TUNEL) method, showed a significant decrease in apoptosis and necrosis of hepatocytes in folic acid-treated group. Histopathological examination of the liver revealed that folic acid protected from severe hepatic degeneration from IIR injury. The biochemical parameters like alanine transaminases and aspartate transaminases were significantly decreased in folic acid-treated group compared to IIR group. In conclusion, folic acid afforded significant protection against IIR injury due to its ability to inhibit IIR-induced apoptosis.