Sodium thiosulfate attenuates liver injury in a rat model of sepsis by modulating ferroptosis and oxidative stress.

ABSTRACT: Sepsis is a dysregulated immune response to infection that can present with a pro-inflammatory endotype in which the ischemia/reperfusion injury leads to excessive production of reactive oxygen species (ROS), inflammatory mediators and the activation of cell death mechanisms. Sodium thiosulfate (STS) is a hydrogen sulfide producing agent that could reduce ischemia/reperfusion injuries induced ROS, inflammation and cell death. We used the peritoneal contamination and infection model in adult rats to induce sepsis. Animals from the treatment groups received either Trolox, an antioxidant medication or STS in doses of 500mg/kg b.w. (STS500 group) or 1000mg/kg b.w. (STS1000 group). Additionally all rats received fluid resuscitation therapy, antibiotic therapy and analgesic treatment. After 48 h

SUBMITTER: Mitre AO 

PROVIDER: S-EPMC12770340 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature