ALT, AST, bile γGT, bile glucose, histopathology, hepatocyte apoptotic activity, apoptotic-related protein Fas, and one-week survival
(i) ALT, AST, apoptotic activity, and Fas (ii) bile γGT, and bile glucose (iii) inflammation and necrosis on histopathology and improved animal survival
ALT, AST, LDH, MDA, SOD, GSH-, MPO, TNF-α expression, MIP-2 expression, histopathology, NO, i-NOS expression, and e-NOS expression
(i) ALT, AST, and LDH (ii) MDA and MPO (iii) TNF-α and MIP-2 expression (iv) SOD, GSH-, and improved hepatic morphology (v) NO and i-NOS and e-NOS expression
Inhibition of neutrophil recruitment and activation, i-NOS and e-NOS-mediated NO production
ALT, AST, NF-κB p65 expression, SOD, apoptotic index, and light and electron microscopy
(i) ALT and AST (ii) NF-κB p65 expression and apoptotic index (iii) SOD (iv) Lower degree of sinusoid congestion and neutrophilic infiltration, lower degree of disruption of nuclear and mitochondrial membranes, and lower degree of degranulation of endoplasmic reticulum
Modulation of apoptotic cascade and maintenance of mitochondrial ultrastructure and function
ALT, MDA, SOD, NO, e-NOS, TNF-α, ICAM-1, HIF-1α, PI3K-Akt, and histopathology
(i) ALT, MDA, TNF-α, and ICAM-1 (ii) SOD, NO, and e-NOS (iii) HIF-1α and PI3K-Akt (iv) Lower scores of cytoplasmic vacuolization, sinusoidal congestion, and hepatocyte necrosis
Suppression of proinflammatory mediators and adhesion molecules, e-NOS-mediated NO production through PI3K-Akt, and upregulation of HIF-1α through NO
ALT, AST, MDA, SOD, HO-1 expression, histopathology, and electron microscopic examination
(i) ALT, AST, and MDA (ii) SOD and HO-1 expression (iii) Decreased vacuolization, sinusoidal congestion and hepatocyte necrosis, and decreased evidence of chromatin damage and mitochondrial disruption
ALT, apoptotic index, 4-HNE modified protein, cytochrome c release from mitochondria, and change of mitochondrial membrane potential
(i) ALT, apoptotic count, and 4-HNE modified protein (ii) Attenuated cytochrome c release from mitochondria and preservation of mitochondrial membrane potential
Inhibition of mitochondrial permeability transition pore opening, preservation of the electrochemical gradient across the inner mitochondrial membrane, and inhibition of release of proapoptotic solutes like cytochrome c
ALT, gene expression analysis after RNA extraction, and quantitative real-time PCR
(i) ALT not different from control (ii) Upregulation of genes involved in DNA binding and transcription, cellular membrane function, and apoptosis and metabolic processes
(i) ALT not different from control, variable kinetics of IL-6, and TNF-α below detection limit at all time points (ii) NVR (iii) apoptotic cell profiles (insignificantly)
AST (peak postop levels), EGD, histopathology, evidence of apoptosis or autophagy, postop morbidity and mortality, and one-year patient and graft survival
(i) Less severe injury on histology (ii) Increased autophagy (iii) No difference in median postop AST, EGD, apoptosis, postop morbidity and mortality, and one-year patient and graft survival