Attenuation of Liver Ischemia/Reperfusion Induced Apoptosis by Epigallocatechin-3-Gallate Via Down-Regulation of NF-κB and c-Jun Expression

摘要: Introduction Hepatic ischemia/reperfusion (I/R) activates Kupffer cells and initiates severe oxidative stress with enhanced production of reactive oxygen species (ROS) tumor necrosis factor-alpha (TNF-α). ROS TNF-α mediate the expression nuclear factors kinases, activating signal transduction pathway, triggering apoptosis. The aim our study was to evaluate potential protective effect (-)-epigallocatechin-3-gallate (EGCG) administration in inhibition apoptosis by attenuating NF-κB, c-Jun, caspase-3 a model hepatic I/R. Materials Methods Thirty Wistar rats were allocated into three groups. Sham operation, I/R, I/R-EGCG 50 mg/kg. ischemia induced for 60 min Pringle's maneuver. Malondialdehyde (MDA), myeloperoxidase (MPO), light histology, scanning electron microscopy, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), immunocytochemistry caspase-3, analysis on liver specimens aspartate (AST), alanine (ALT) transferases serum, performed 120 min after reperfusion. Results Apoptosis as indicated TUNEL widely expressed I/R group but very limited EGCG treated group. Liver stained positive NF-κB c-Jun failed be MDA, MPO, AST, ALT showed marked increase significant decrease Significant alterations observed histology transmission microscopy whilst pretreatment resulted parenchymal preservation. Conclusions Administration is likely inhibit I/R-induced protect down-regulating pathways.