Human exposure to nanoparticles became unavoidable secondary to their massive
involvement in a multitude of industrial applications. Zinc oxide nanoparticles (ZnONPs) are one
of the most commonly used metal oxide nanoparticles in biological applications. Naringenin
(NAR), a citrus-derived flavonoid, has favorable biological properties that promote human
health. The present study was carried out to investigate the possible defensive role of NAR
versus ZnONPs provoked hepatic injury in rats through an evaluation of liver enzymes, hepatic
biomarkers of oxidative stress, inflammatory process, apoptotic cell death along with
histopathological examination of liver tissue. Therefore, 32 adult rats were randomly divided into
four equal groups as control, NAR, ZnONPs and co-treated ZnONPs with NAR groups. All
treatments were administered for 14 days. Our results showed that ZnONPs induced hepatic
injury as documented by the marked increased hepatic enzymes activities, disturbed hepatic
oxidant/antioxidant balance, increased hepatic inflammatory reactions, in addition to, extensive
hepatic morphological alterations, marked collagen fibers accumulation as well as
overexpression of apoptotic BAX and the noticeable intensified positive nuclear staining for
nuclear factor Kabba-b (NF-κB) in hepatic tissues. Concurrent NAR supplement to ZnONPstreated
rats significantly declined liver enzymes activities, restored oxidant/antioxidant balance,
reversed inflammation, induced fewer collagen fibers accumulation, and antagonized BAXmediated
apoptotic cell death in hepatic tissues. We concluded that concurrent NAR supplement
to ZnONPs treated rats improved hepatic function and structure by its antioxidant, antiinflammatory
and antiapoptotic potentials.