An APE1 Inhibitor Reveals Critical Roles of APE1 Redox Function in Pathogenesis of Chronic Rhinosinusitis and Novel Therapeutics

We demonstrated that the Apurinic/apyrimidinic endonuclease 1 (APE1) redox inhibitor, C10, effectively blocked Type 2 inflammation and improved chronic rhinosinusitis (CRS) pathology in a mouse model. Overall design: Chronic rhinosinusitis (CRS) mice model To establish CRS mice model, mice in CRS group were treated intranasally with 20µg Papain (Sigma-Aldrich, P5306-25MG, USA) which was dissolved in 20µL phosphate buffer saline (PBS) on days 0-2 and 7-11. Drug treatment The treatment dosage of C10 (MCE, HY-19357, CHN) drug solution for intranasal administration in CRS mice were 10 mg/mL, with bilateral administration (10 µl/side, bilateral intranasal instillation). Starting from the initial administration of papain, treatment was continued for 10 consecutive days, with once-daily application. The concentration 10 ng/mL of IL-13 (MCE, HY-P72795, CHN) was used to stimulate Beas-2b and HNECs for 48 hours.