There is little information about the hepatoprotective effects of
gallic acid against
ischemia-reperfusion (I/R) damage. Animals were subjected to I/R.
Gallic acid at doses of 50 and 100 mg/kg
body weight (bw) were injected as a single dose prior to
ischemia. Liver tissue homogenates were used for the measurement of
malondialdehyde (MDA),
catalase (CAT) and
glutathione peroxidase (GPx) levels. At the same time
alanine aminotransferase (ALT),
aspartate aminotransferase (AST) and
lactate dehydrogenase (LDH) were assayed in serum samples and compared statistically. While the ALT, AST, LDH activities and MDA levels were significantly increased, CAT and GPx activities significantly decreased in only I/R-induced control rats compared to normal control rats (P < 0.05). Treatment with
gallic acid at a dose of 100 mg/kg bw significantly decreased the ALT, AST, LDH activities and MDA levels, and markedly increased activities of CAT and GPx in tissue homogenates compared to I/R-induced rats with no treatment group (P < 0.05). In oxidative stress generated by hepatic
ischemia-reperfusion,
gallic acid contributes partially an alteration in the delicate balance between the scavenging capacity of
antioxidant defense systems and
free radicals in favour of the
antioxidant defense systems in the body.