Antihepatoma and Liver Protective Potentials of Ganoderma Lucidum (靈芝 Ling Zhi) Fermented in a Medium Containing Black Soybean (黑豆 Hēi Dòu) and Astragalus Membranaceus (生黃耆 Shēng Huáng Qí)

• Main Authors: Zheng-Yuan Su, Lucy Sun Hwang, Been-Huang Chiang, Lee-Yan Sheen
• Format: Article
• Language: English
• Published: Elsevier 2013-04-01
• Series: Journal of Traditional and Complementary Medicine
• Subjects: Antihepatoma activity; Astragalus membranaceus; Black soybean; Fermentation; Ganoderma lucidum; Liver protective function
• Online Access: http://www.sciencedirect.com/science/article/pii/S2225411016301754

The antihepatoma activity and liver protective function of the fermentation products (5 L fermenator) of Ganoderma lucidum (GL; 靈芝 Ling Zhi) cultivated in a medium containing black soybean (BS; 黑豆 Hēi Dòu) and Astragalus membranaceus (AM; 生黃耆 Shēng Huáng Qí) at different fermentation temperatures were investigated in this study. Hep 3B cells pretreated with lovastatin were used to study the antihepatoma activity, and possible active components were analyzed by reverse-phase high-performance liquid chromatography. Carbon tetrachloride (CCl4)-induced primary rat hepatocyte injury was further used to evaluate the liver protective activity of the fermentation products. While all the GL broth filtrates do not inhibit the growth of Hep 3B cells, the ethanolic extract from GL-2 mycelia (GL-2-mE), cultivated in the medium containing BS (50 g/L) and AM (20 g/L) at 24 °C for 11 days showed the best antihepatoma activity (IC50 26.6 μg/mL) than the other ethanolic extracts from GL mycelia, GL fruiting body, BS, and AM did. The antihepatoma activities were correlated with some unknown active components in these samples. Furthermore, GL-2-mE (100 μg/mL) without harmful effect on the growth of normal primary rat hepatocytes significantly maintained cell viability, reduced lactate dehydrogenase leakage, lowered lipid peroxidation, and increased glutathione peroxidase and glutathione S-transferase activities in the CCl4-induced damaged primary rat hepatocytes.