Expression of Thioredoxin Family Proteins During Perinatal Asphyxia

Abstract

Background: Alterations in the gas exchange in the placenta and fetus lungs malfunction in humans can lead to perinatal asphyxia (PA). Every organ in the body is affected by PA, yet it is particularly deleterious for the central nervous system (CNS). The reoxygenation that follows a PA event produces a great quantity of ROS, which can ultimately lead to irreversible changes in the redox balance. Thioredoxins (Trxs) are a group of proteins that are closely involved in redox regulation and have been recognized as the most important regulators of the thiol redox state. In the present study, we analyze the changes in Trxs expression and distribution in hippocampus, striatum and cerebellum caused by PA, in 30 days-old rats.

Method: The model for common carotid artery ligation used in this study mimics PA in murine animals. On post-natal day seven, Sprague-Dawley rats were subjected to a ligation of the common carotid artery, followed by nitrogen exposure (HI group) or sham-operation procedures (ctrl group). Animals were euthanized, and the obtained samples were analyzed by Western blot, ELISA and immunohistochemistry.

Results and conclusions: Our data showed changes in the expression of Prx2, Trx1, Trx2, Grx2, Grx5 and TrxR1. This study shows the complexity of the expression and distribution of Trxs in the different areas of the CNS and sheds light on the importance of some of the Trxs family members in PA, and thus, as possible targets for therapeutic interventions.