PhD Scientific Days 2025

Budapest, 7-9 July 2025

Poster Session II. - W: Conservative Medicine

phd student

Name of the presenter

Zrufkó Réka

Institute/workplace of the presenter

Doctoral College Semmelweis University Károly Rácz Conservative Medicine Division

Authors

Réka Zrufkó1, Beáta Szebeni1,2, Apor Veres-Székely1, Csenge Pajtók2, Péter Bokrossy2, Csenge Szász2, Attila J. Szabó1,2, Ádám Vannay1,2, Domonkos Pap1,2

1: Pediatric Center, MTA Center of Excellence, Semmelweis University
2: HUN-REN–SU Pediatrics and Nephrology Research Group

Text of the abstract

Aims: Sepsis-induced acute kidney injury (AKI) is a condition associated with significant morbidity and mortality, for which there is no effective therapy. A central elements of its pathomechanism are oxidative stress and inflammation. The antioxidant and anti-inflammatory role of the Parkinson’s disease 7 (PARK7) molecule is known, but it has not been investigated as a potential therapeutic target in sepsis-induced AKI. Therefore, our aim was to explore the role of PARK7 in the pathomechanism of the disease.
Methods: We investigated the effect of the compound Comp23, which activates the protective functions of PARK7, on apoptosis induced by bacterial lipopolysaccharide (LPS) and H2O2 in HEK293 kidney epithelial cells. We also examined the effect of Comp23 on oxidative stress induced by LPS and H2O2 and its molecular markers in HEK293 cells. We explored the anti-inflammatory effect of the compound Comp23 on LPS and H2O2 activated immune cells. We investigated the effect of PARK7 activation on inflammation, oxidative stress, and kidney function damage (creatinine, BUN) during LPS-induced acute kidney injury in vivo.
Results: We demonstrated that PARK7 activation with Comp23 reduces LPS and H2O2-induced cell death and oxidative stress in HEK293 cells. Our results showed that Comp23 activation decreases the production of inflammatory cytokines induced by LPS and H2O2 in immune cells. We also showed that the Comp23 decreased inflammation and oxidative stress in the kidneys during LPS-induced sepsis. Additionally, treatment with Comp23 reduced serum creatinine and BUN levels in LPS-treated animals.
Conclusion: Our studies have pointed out that the PARK7 molecule is a potential therapeutic target in sepsis-induced acute kidney injury (AKI) through the activation of antioxidant and anti-inflammatory mechanisms.