protective effect of folic acid against apoptosis induced by ischemia/reperfusion injury in rat liver

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 bcl-2 in i/r in rat liver. eighteen wister rats were divided into sham-operated controlgroup (c) (n=6), i/r group (n=6), folic acid treated group which received 1 mg/kg/day folic acid by oral route for 7 days before induction of i/r (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 i/r group. quantification of apoptotic and necrotic hepatocytes, measured by fluorescence microscopy and terminal deoxynucleotidyl transferase (tdt)-mediated dudp-biotin nick end labeling (tunel) method, showed a significant decrease in apoptosis and necrosis of hepatocytes in folic acid-treated group. histopathologi-cal examination of the liver revealed that folic acid protected from severe hepatic degeneration from i/r injury. the biochemical parameters like alanine transaminases and aspartate transaminases were significantly decreased in folic acid-treated group compared to i/r group. in conclusion, folic acid afforded significant protection against i/r injury due to its ability to inhibit i/r-induced apoptosis.