الفهرس | Only 14 pages are availabe for public view |
Abstract Acute liver injury (ALI) is a life-threatening syndrome accompanied by overwhelming oxidative stress, inflammation and apoptosis.The present investigation was directed to estimate the potential hepatoprotective effects of bromelain (Brom) compared with silymarin (SLM) as a reference standard in d-galactosamine(GalN)-induced ALI in rats as well as to explore the underlying protective mechanisms. Brom (20 & 40 mg/kg/p.o.) and SLM (100 mg/kg/p.o.) were administered to the experimental rats once daily for ten successive days.ALI was induced in male Wistar rats by a single injection of GalN (400 mg/kg/i.p.) on the 8th day of the experiment.Pretreatment with Brom improved the liver functions and histolopathological changes induced by GalN. Brom amended GalN-induced oxidative stress by promoting protein expression of the phosphorylatednuclear factor erythroid 2{u2013}related factor 2 (p-Nrf2) along with increasing the hepatic antioxidant enzymes; including heme oxygenase-1 (HO-1) and NADPH quinone oxidoreductase 1 (NQO1). Likewise, Brom ameliorated GalN-induced inflammation by decreasing hepaticnuclear factor kappa B p65 (NF-mB p65) and tumor necrosis factor-Ü (TNF-Ü) contents, besdies improvement of the apoptosis-related proteins by reducing caspase-8 and caspase-9 in the liver. Moreover, Brom modulated glycogen synthase kinase-3Ý/ nuclear factor erythroid 2-related factor 2 (GSK3Ý/Nrf2) axis and activated the sirtuin-1/liver kinase B1/AMP-activated protein kinase (SIRT1/LKB1/AMPK) signaling pathway.Taken together, the present results unveil that Brom is capable of ameliorating GalN-induced ALI |