Protective Effect of Folic Acid against Apoptosis Induced by Ischemial Reperfusion Injury in Rat Liver

The anti-apoptotic gene bcl-2 is located in mitochondria, but it is uncertainwhether 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 bel2in iir in rat liver. eighteen wister rats were divided into sham-operated controlgroup (c) (n=6), ijr group (n=6) , folic acid treated group which received img/kg/day folic acid by oral route for 7 days before induction of iir (n=6). bcl-2expression was measured by rt-pcr and western blot methods. folic acidsignificantly increased bcl-2 mrna expression in comparison to the iir group.quantification of apoptotic and necrotic hepatocytes, measured by fluorescencemicroscopy and terminal deoxynucleotidyl transferase (tdt)-mediated dudpbiotinnick end labeling (tunel) method, showed a significant decrease inapoptosis and necrosis of hepatocytes in folic acid-treated group. histopathologicalexamination of the liver revealed that folic acid protected from severe hepaticdegeneration from iir injury. the biochemical parameters like alanine transaminasesand aspartate transaminases were significantly decreased in folic acid-treated groupcompared to iir group. in conclusion, folic acid afforded significant protection againstiir injury due to its ability to inhibit iir-induced apoptosis.