USP13 reduces septic mediated cardiomyocyte oxidative stress and inflammation by inducing Nrf2

Background: Sepsis is a common cardiovascular complication that can cause heart damage. The regulatory role of ubiquitin-specific peptidase 13 (USP13) on erythroid 2–related factor 2 (Nrf2) has been reported, but its in septic cardiomyopathy remains unclear.Methods: Sprague Dawley (SD) rat model myocardial injury was constructed by lipopolysaccharides (LPS). serum lactate dehydrogenase (LDH) and creatine kinase (CK) levels were detected, the mRNA protein expression Nrf2 USP13 tissues detected real-time quantitative reverse transcription PCR (qRT-PCR) western blot (WB), at treatment time 3 h, 6 12 h alsodetected. cell viability USP13, Nrf-2 heme oxygenase-1 (HO-1) H9C2-treated cells LPS oxidative stress level inflammatory response H9C2 enzyme-linked immunosorbent assay (ELISA) WB.Results: results showed downregulated tissues, increased vitro after treated with LPS. Overexpression further induced to reduce apoptosis, stress, factors.Conclusion: In conclusion, this study demonstrated overexpression reduced apoptosis. Further studies LPS-induced inflammation inducing Nrf2.