Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/6589
Title: Myrica rubra extracts protect the liver from CCl₄-induced damage
Authors: Xu, L
Gao, J
Wang, Y
Yu, W
Zhao, X
Yang, X
Zhong, Z
Qian, ZM
Keywords: Dependent anion channel
Mitochondrial permeability transition
Tetrachloride-induced hepatotoxicity
Carbon tetrachloride
Natural medicines
Skeletal-muscle
Cell life
Injury
Mice
Death
Issue Date: 2011
Publisher: Hindawi Publishing Corporation
Source: Evidence-based complementary and alternative medicine, 2011, v. 2011, 518302, p. 1-8 How to cite?
Journal: Evidence-based complementary and alternative medicine 
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.
URI: http://hdl.handle.net/10397/6589
ISSN: 1741-427X
EISSN: 1741-4288
DOI: 10.1093/ecam/nep196
Rights: Copyright © 2011 Lizhi Xu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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