Functionalized selenium nanoparticles ameliorated acetaminophen-induced hepatotoxicity through synergistically triggering PKCδ/Nrf2 signaling pathway and inhibiting CYP 2E1

Selenium nanoparticles (SeNPs) have been demonstrated potential for use in diseases associated with oxidative stress. Functionalized SeNPs lower toxicity and higher biocompatibility could bring better therapeutic activity clinical application value. Herein, this work was conducted to investigate the protective effect of Pleurotus tuber-regium polysaccharide-protein complex funtionnalized (PTR-SeNPs) against acetaminophen (APAP)-induced injure HepG2 cells C57BL/6J mouse liver. Further elucidation underlying molecular mechanism, particular their modulation Nrf2 signaling pathway also performed. The results showed that PTR-SeNPs significantly ameliorate APAP-induced injury as evidenced by a range biochemical analysis, histopathological examination immunoblotting study. hosphorylate activate PKCδ, depress Keap1, increase nuclear accumulation Nrf2, resulting upregulation GCLC, GCLM, HO-1 NQO-1 expression. Besides, suppressed biotransformation APAP generate intracellular ROS through CYP 2E1 inhibition, restoring mitochondrial morphology. Furthermore, induced hepatotoxicity weakened depleted in vivo, indicating pivotal role mediated hepatoprotective efficacy. Being hepatic protectant, serve new source selenium supplement health-promting biomedical applications.