Evaluation of immunohistochemical expression of GSTA1 and GSTP1 isoenzymes before and after treatment of Trx and L-NAME in experimental hepatic ischemia/reperfusion model

Abstract

Ischemia/reperfusion (I/R) causes formation of Reactive Oxygen Species (ROS) in tissues, in response to which injured cells improve a number of defense mechanisms including Glutathione S-Transferases (GSTs). The aim of this study was to investigate the expressions of GSTA1 and GSTP1 following Thioredoxin (Trx) and N-nitro-L-arginine methyl ester (L-NAME) treatment in a rat model of hepatic I/R model. A total of 50 Wistar rats were randomly allocated into 5 groups: sham (n = 10), control (I/R) (n = 10), Trx (n = 10), L-NAME (n = 10), and Trx+L-NAME (n = 10). With an exception to those in sham group, all rats were subjected to a hepatic ischemia process for an hour and then subsequent reperfusion. GSTA1 and GSTP1 expressions in the liver tissues were determined by immunohistochemical method. The GSTA1 expression was absent in sham group while varying degrees of expression occurred in other groups. The GSTA1 expression was significantly higher in Trx/L-NAME group compared to other groups (p <0.05). GSTP1 expression was no difference between groups (p >0.05). As a result, we think that GSTA1 expression may have increased in response to I/R as a part of the liver oxygen radical scavenging process.