Abstract
BACKGROUND AND PURPOSE: Voltage dependent anion channel (VDAC) plays an important role in triggering the opening of the mitochondrial permeability transition pore (PTP) that leads to mitochondrial damage and induce apoptic or necrotic cell death. In the present study, the methanolic extract of Amomum subulatum Roxb. seeds (MEAS) was used to examine its effect on VDAC. Aminotransferase activity, mitochondrial membrane potential, calcium-induced liver MPT, and VDAC expression were used to evaluate the hepato protective effect of MEAS. RESULTS: Pretreatment of mice with MEAS (100 and 300 mg/kg) significantly blocked the CCl(4)-induced increase in AST and ALT activities. Pretreatment with MEAS showed significant preservation of mitochondrial membrane potential as compared to CCl(4) control demonstrating the mitochondrial protection. In addition, pretreatment with MEAS at various concentrations exerted a dose-dependent effect against sensitivity to mitochondrial swelling induced by calcium. In addition, MEAS (300 mg/kg) significantly increased the transcription and translation of VDAC. CONCLUSION: Our data suggest that MEAS significantly prevents the damage to liver mitochondria through regulation of VDAC expression.