Myrica rubra extracts protect the liver from CCl₄-induced damage

Abstract

The relationship between the expression of mitochondrial voltage-dependent anion channels (VDACs) and the protective effects of Myrica rubra Sieb. Et Zucc fruit extract (MCE) against carbon tetrachloride (CCl₄)-induced liver damage was investigated. Pretreatment with 50 mg kg⁻¹, 150 mg kg⁻¹ or 450 mg kg⁻¹ MCE significantly blocked the CCl₄-induced increase in both serum aspartate aminotransferase (sAST) and serum alanine aminotransferase (sALT) levels in mice (P < .05 or .01 versus CCl₄ group). Ultrastructural observations of decreased nuclear condensation, ameliorated mitochondrial fragmentation of the cristae and less lipid deposition by an electron microscope confirmed the hepatoprotection. The mitochondrial membrane potential dropped from −191.94 ± 8.84 mV to −132.06 ± 12.26 mV (P < .01) after the mice had been treated with CCl₄. MCE attenuated CCl₄-induced mitochondrial membrane potential dissipation in a dose-dependent manner. At a dose of 150 or 450 mg kg⁻¹ of MCE, the mitochondrial membrane potentials were restored (P < .05). Pretreatment with MCE also prevented the elevation of intra-mitochondrial free calcium as observed in the liver of the CCl₄-insulted mice (P < .01 versus CCl₄ group). In addition, MCE treatment (50–450 mg kg⁻¹) significantly increased both transcription and translation of VDAC inhibited by CCl₄. The above data suggest that MCE mitigates the damage to liver mitochondria induced by CCl₄, possibly through the regulation of mitochondrial VDAC, one of the most important proteins in the mitochondrial outer membrane.