Antioxidant and hepatoprotective effects of Korean ginseng extract GS-KG9 in a D-galactosamine-induced liver damage animal model

• Published in: Nutrition research and practice Vol. 14; no. 4; pp. 334 - 351
• Main Authors: Jo, Yun Ho, Lee, Hwan, Oh, Myeong Hwan, Lee, Gyeong Hee, Lee, You Jin, Lee, Ji Sun, Kim, Min Jung, Kim, Won Yong, Kim, Jin Seong, Yoo, Dae Seok, Cho, Sang Won, Cha, Seon Woo, Pyo, Mi Kyung
• Format: Journal Article
• Language: English
• Published: 한국영양학회 01.08.2020; The Korean Nutrition Society and the Korean Society of Community Nutrition
• Subjects: Original Research; 생활과학; galactosamine; liver fibrosis; liver; Panax ginseng; oxidative stress
• ISSN: 1976-1457; 2005-6168
• DOI: 10.4162/nrp.2020.14.4.334

BACKGROUND/OBJECTIVESThis study was designed to investigate the improvement effect of white ginseng extract (GS-KG9) on D-galactosamine (Ga1N)-induced oxidative stress and liver injury. SUBJECTS/METHODSSixty Sprague-Dawley rats were divided into 6 groups. Rats were orally administrated with GS-KG9 (300, 500, or 700 mg/kg) or silymarin (25 mg/kg) for 2 weeks. The rats of the GS-KG9- and silymarin-treated groups and a control group were then intraperitoneally injected Ga1N at a concentration of 650 mg/kg for 4 days. To investigate the protective effect of GS-KG9 against GalN-induced liver injury, blood liver function indicators, anti-oxidative stress indicators, and histopathological features were analyzed. RESULTSSerum biochemical analysis indicated that GS-KG9 ameliorated the elevation of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) in GalN-treated rats. The hepatoprotective effects of GS-KG9 involved enhancing components of the hepatic antioxidant defense system, including glutathione, glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT). In addition, GS-KG9 treatment inhibited reactive oxygen species (ROS) production induced by GalN treatment in hepatocytes and significantly increased the expression levels of nuclear factor erythroid-2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) proteins, which are antioxidant proteins. In particular, by histological analyses bases on hematoxylin and eosin, Masson's trichrome, α-smooth muscle actin, and transforming growth factor-β1 staining, we determined that the administration of 500 mg/kg GS-KG9 inhibited hepatic inflammation and fibrosis due to the excessive accumulation of collagen. CONCLUSIONSThese findings demonstrate that GS-KG9 improves GalN-induced liver inflammation, necrosis, and fibrosis by attenuating oxidative stress. Therefore, GS-KG9 may be considered a useful candidate in the development of a natural preventive agent against liver injury.