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.