Protective Effect of Panax notoginseng Saponins on Acute Ethanol-Induced Liver Injury Is Associated with Ameliorating Hepatic Lipid Accumulation and Reducing Ethanol-Mediated Oxidative Stress

• Published in: Journal of agricultural and food chemistry 2015-03, Vol.63 (9), p.2413-2422
• Main Authors: Ding, Ren-Bo, Tian, Ke, Cao, Yi-Wei, Bao, Jiao-Lin, Wang, Meng, He, Chengwei, Hu, Yuanjia, Su, Huanxing, Wan, Jian-Bo
• Format: Article
• Language: English
• Subjects: Animals; Chemical and Drug Induced Liver Injury - drug therapy; Chemical and Drug Induced Liver Injury - metabolism; Drugs, Chinese Herbal - administration & dosage; Ethanol - adverse effects; Glutathione - metabolism; Humans; Liver - drug effects; Liver - metabolism; Male; Malondialdehyde - metabolism; Mice; Mice, Inbred C57BL; Oxidative Stress - drug effects; Panax notoginseng - chemistry; Reactive Oxygen Species - metabolism; Saponins - administration & dosage; Triglycerides - metabolism
• ISSN: 0021-8561; 1520-5118
• DOI: 10.1021/jf502990n

The aim of present study was to evaluate the effects of Panax notoginseng saponins (PNS) against acute ethanol-induced liver injury and further to elucidate its probable mechanisms. Mice were treated with PNS (100 or 300 mg/kg) once daily for seven consecutive days priors to ethanol gavage (4.7 g/kg) every 12 h for a total of three doses. Acute alcohol gavage dramatically significantly increased serum activities of alanine aminotransferase (ALT) (23.4 ± 5.0 IU/L vs 11.7 ± 4.1 IU/L) and aspartate aminotransferase (AST) (52.6 ± 14.9 IU/L vs 31.1 ± 12.9 IU/L), and hepatic triglyceride level (4.04 ± 0.64 mg/g vs 1.92 ± 0.34 mg/g), these elevations were significantly diminished by pretreatment with PNS at dose of 100 mg/kg or 300 mg/kg. Alcohol exposure markedly induced the lipolysis of white adipose tissue (WAT), up-regulated protein expression of the phosphorylated hormone-sensitive lipase (p-HSL, p < 0.01), and total HSL (p < 0.01), and enhanced fatty acid uptake capacity in liver as indicated by increasing hepatic CD36 expression (p < 0.01), these effects were attenuated by PNS treatment. Additionally, PNS suppressed the elevation of reactive oxygen species (ROS) production and malondialdehyde (MDA) content, reduced TNF-α and IL-6 levels, restored glutathione (GSH) level, enhanced the superoxide dismutase (SOD) activity in liver, and abrogated cytochrome P450 2E1 (CYP2E1) induction. These data demonstrated that pretreatment with PNS protected against acute ethanol-induced liver injury, possibly through ameliorating hepatic lipid accumulation and reducing CYP2E1-mediated oxidative stress. Our findings also suggested that PNS may be potential to be developed as an effective agent for acute ethanol-induced liver injury.