RESUMEN
OBJECTIVE: To explore the relationship between the protection of hydrogen sulfide (H(2)S) against hepatic ischemia-reperfusion injury and thioredoxin system in rats. METHODS: Eighteen adult rats were divided randomly into 3 groups, i.e. sham, ischemia-reperfusion (IR) and sodium hydrogen sulfide (NaHS). The rats in the IR and NaHS groups were subjected to ischemia for 60 min and followed by reperfusion for 6 hours. In the NaHS group, there was an intraperitoneal dosing of NaHS (28 µmol/kg) at 5 min pre-reperfusion. Blood samples were collected for the measurements of alanine transaminase (ALT) and aspartate transaminase (AST). Liver tissue samples were collected for measurements of Trx and TrxR activity by enzyme-linked immunosorbent assay (ELISA), Western blot detection of Trx system proteins and thioredoxin interacting protein (TXNIP) expression. Hematoxylin-eosin staining was used to observe the hepatic histopathological changes. RESULTS: Compared with the sham group, increased activities of ALT and AST were found in the IR group, accompanied by aggravated pathological injury. In addition, NaHS administrated at pre-reperfusion could alleviate hepatic injury. Compared with the sham group, the IR group had decreased Trx activity and Trx1 protein expression and increased TXNIP protein expression (P < 0.05) while the NaHS group had increased Trx activity and Trx1 protein expression and decreased TXNIP protein expression (P < 0.05). It indicated that the postconditioning with H(2)S could reduce the inhibition of Trx system and boost tissue antioxidant capacity. CONCLUSION: Hydrogen sulfide postconditioning can enhance the cellular Trx system and play a protective role in hepatic ischemia-reperfusion injury.