EFFECTS OF NF-?B AND NRF2 MODULATORS ON REACTIVE OXYGEN AND NITROGEN SPECIES PRODUCTION IN RAT HEARTS FOLLOWING SURGICAL TRAUMA UNDER PROLONGED STRESS

This study is of great relevance due to the growing interest in understanding the mechanisms underlying cardiovascular complications following surgery and trauma, particularly in the context of posttraumatic stress disorder. A commonly used experimental model for the latter is single prolonged stress (SPS), which includes restraint, forced swimming, and ether anesthesia. In this work, we evaluated the effects of modulators of transcription factors NF-κB (BAY 11-7082) and Nrf2 (sulforaphane) on the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in the myocardium of rats subjected to SPS and subsequent surgical trauma. Quantitative analysis of ROS and RNS production was carried out using electron paramagnetic resonance (EPR) spectroscopy and specific spin traps. The results revealed that trauma and stress led to a marked increase in ROS and RNS generation. BAY 11-7082 administration reduced ROS levels but had a minimal effect on RNS, while sulforaphane significantly attenuated both ROS and RNS production. These findings indicate that targeting Nrf2 pathways may offer a more comprehensive cardioprotective strategy in stress-related cardiac injury.