Alteration of AP-endonuclease1 expression in curcumin-treated fibrotic rats.

摘要: Abstract Background. Apurinic/apyrimidinic endonuclease1/ redox factor-1 (APE1/Ref-1) is a multifunctional protein involved in DNA base excision repair and regulation of many transcription factors. It an important pro-survival activated response to oxidative stress. Increased level this essential sensi¬tive correlates closely with cellular survival against insults. Curcumin (diferuloylmethane) naturally occurring compound derived from turmeric has attracted interest because its anti-inflamma¬tory, anti-oxidative, chemopreventive activities. Material methods. The current study evaluates the vivo role curcumin protecting treating liver injury fibrogenesis caused by carbon tetrachloride (CCl 4 ) rats. also addresses possible involvement APE1 hepatoprotection. Analysis expression was performed at mRNA levels reverse trans¬criptase (RT)-PCR western blotting respectively. Profile HSCs-activation related genes were assayed RT-PCR pro-inflammatory cytokines determined enzyme-linked immune assays. Results. Here we show that oral administration accompanied robust increase levels, improved histological architecture rat liver. In addition, attenuated stress increasing content hepatic glutathione within normal values, leading re¬duction lipid hydroperoxide. remarkably suppressed inflammation reducing le¬vels inflammatory cytokines, including tumor necrosis factor-α (TNF-α), nuclear factor-kappa B (NF-kB) interleukin-6 (IL-6). inhibited stellate cells (HSCs) activation elevating PPARγ abundance transforming growth factor-β (TGF-β). We found adminis¬tration 200 mg/kg dose not only protected CCl 4- induced injury, but re¬sulted more than two-fold induction group. Conclusions. can be concluded reduced markers damage rats treated , conco¬mitant elevation indicating protective effect unknown mechanism. enzymes may novel strategy for protection injury.