Involvement of both intrinsic and extrinsic pathways in hepatoprotection of arjunolic acid against cadmium induced acute damage in vitro

摘要: Abstract Cadmium (Cd) is one of the ubiquitous environmental pollutants and responsible for various organ pathophysiology including hepatic disorders. It extremely toxic even in low concentrations bioaccumulate organisms. The present study has been carried out to investigate cytoprotective role arjunolic acid (AA), a tri terpenoid saponin, against Cd induced oxidative impairment cell death murine hepatocytes. Administration cadmium (30 μM), form chloride (CdCl2) 2 h, significantly enhanced ALT, ALP LDH leakage, increased reactive oxygen species (ROS) production, reduced hepatocytes viability altered antioxidant status by reducing intracellular GSH level, anti-oxidant enzymes activity increasing GSSG lipid peroxidation. Evidence Cd-induced nature was sought flow cytometric analysis. Signal transduction studies revealed that markedly levels caspase-9, -8, -3, Fas Bid, decreased mitochondrial membrane potential, cytochrome c release cytosol, disturbed Bcl-2 family protein balance, cleaved PARP ultimately led apoptotic death. Results showed could trigger both intrinsic extrinsic pathways. In addition, NF-κB nuclear translocation association with IKKα/β phosphorylation IκBα degradation. Simultaneous treatment AA (200 μM), however, stress, attenuated protects from Combining, data suggest dysfunction apoptosis might be supported ROS formation mediated via activation NF-κB. treatment, on other hand, mitochondrion-dependent independent signaling