Myrica rubra extract protects the liver from chemically-induced damage. - GreenMedInfo Summary
Myrica rubra Extracts Protect the Liver from CCl4-Induced Damage.
Evid Based Complement Alternat Med. 2009 Dec 17. Epub 2009 Dec 17. PMID: 20019074
School of Pharmacy, Jiangsu University, 301 Xue Fu Road Zhenjiang, PRC 212013. E-mail: jingao@NJU.edu.hk. or Zhong-Ming Qian, PhD, Department of Applied Biology&Chemical Technology and Shenzhen Key Laboratory of Chinese Medicine and Molecular Pharmacology, The Hong Kong Polytechnic University, Kowloon, Hong Kong. E- email@example.com.
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 (CCl(4))-induced liver damage was investigated. Pretreatment with 50 mg kg(-1), 150 mg kg(-1) or 450 mg kg(-1) MCE significantly blocked the CCl(4)-induced increase in both serum aspartate aminotransferase (sAST) and serum alanine aminotransferase (sALT) levels in mice (P<0.05 or 0.01 vs CCl(4) 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<0.01) after the mice had been treated with CCl(4). MCE attenuated CCl(4)-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<0.05). Pretreatment with MCE also prevented the elevation of intra-mitochondrial free calcium as observed in the liver of the CCl(4)-insulted mice (P<0.01 vs CCl(4) group). In addition, MCE treatment (50-450 mg kg(-1)) significantly increased both transcription and translation of VDAC inhibited by CCl(4). The above data suggest that MCE mitigates the damage to liver mitochondria induced by CCl(4), possibly through the regulation of mitochondrial VDAC, one of the most important proteins in the mitochondrial outer membrane.