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oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/129802026-10-18T21:13:24Zopenairedrivercom_ebyu_10000col_ebyu_10001

Hepatoprotective and neuroprotective effect of taxifolin on hepatic encephalopathy in ratsOkkay, UfukFerah Okkay, IrmakCicek, BetulAydin, Ismail CagriOzkaraca, MustafaApoptosisHepatic encephalopathyInflammationOxidative stressTaxifolinThioacetamideAnimalsAntioxidantsHyperammonemiaLiverNeuroprotective AgentsQuercetinRatsRats, Wistar8 hydroxydeoxyguanosinealanine aminotransferasealkaline phosphataseammoniaaspartate aminotransferasecaspase 3catalaseglutathioneimmunoglobulin enhancer binding proteininducible nitric oxide synthaseinterleukin 10interleukin 1betalactate dehydrogenasemalonaldehydeprotein Baxprotein bcl 2This study was planned to assess the potential protective effects of taxifolin against thioacetamide-induced hepatic encephalopathy and subsequently to portray its behavioural results. The experimental model was induced with three doses of (200 mg/kg i.p.) thioacetamide and taxifolin (50 and 100 mg/kg, p.o.) was administered for fourteen days. Taxifolin effectively attenuated hepatic encephalopathy through decrease in AST, ALT, ALP and LDH concentrations and improvement of hyperammonemia, and increase in antioxidant capacity by decreasing MDA, ROS, and increasing CAT and GSH. In addition, the expressions of NF-κB, TNF-α, IL-1β, caspase-3 and Bax was down-regulated while IL-10 and Bcl-2 expressions were up-regulated with taxifolin treatment. The recovery was confirmed by downregulation of iNOS and 8-OHdG expressions in our immunohistochemical analysis. Taxifolin treatment reduced the disrupting role of thioacetamide as seen by corrected hyperammonemia as well as preservation of astrocyte and hepatocyte structure. Elevated plus maze and locomotor activity tests also proved that taxifolin might repeal the neurobehavioral disabilities. In conclusion, taxifolin has shown hepatoprotective and neuroprotective roles with antioxidant and anti-inflammatory effects, as well as suppressing the excessive release of ammonia, and it eventually reversed neurobehavioral impairments. Graphical abstract: [Figure not available: see fulltext.]. © 2022, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.Springer2022Articlehttps://rdlopen.rawdatalibrary.net/r/ebyu/12980https://doi.org/10.1007/s11011-022-00952-30885-7490enMetabolic Brain Diseaseinfo:eu-repo/semantics/openAccessinfo:eu-repo/semantics/articlehttps://ebyu-rdlopen.rawdatalibrary.net/tr/items/ebyu/12980