title: Protective effects of ginseng total saponins against hepatic ischemia/reperfusion injury in experimental obstructive jaundice rats.
abstract: BACKGROUND
  Ginseng, the root of Panax ginseng C.A. Meyer (Araliaceae), is one of the most extensively used herbs for stroke and chronic debilitating conditions in East Asian countries. Ginsenosides (GS) are the main bioactive compounds for ginseng's efficacy, but the mechanisms have not been fully clarified.
  
  
  OBJECTIVE
  To investigate hepatoprotective effects of GS against ischemia/reperfusion (IR) injury in the experimental obstructive jaundice rats.
  
  
  METHODS
  GS was fed to cholestatic rats with IR injury daily for 6 d at a dose of 1.10 g/kg. Levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), superoxide dismutase (SOD) and malondialdehyde (MDA) were determined by colorimetric method. Apoptosis was measured quantitatively by the terminal transferase UTP nick end-labeling method. Protein expression of Bax and Bcl-2 was detected by immunohistochemistry.
  
  
  CONCLUSIONS
  After intervention of GS to cholestatic rats with IR injury, the levels of activating blood flow were significantly improved, and the levels of serum ALT were decreased 1.7-times, AST decreased 1.3-times, but SOD activities were increased 1.1-times compared with those of the model rats. It could also reverse histopathological changes and inhibit IR-induced apoptosis of hepatic tissues via decrease of Bax/Bcl-2 ratio (from 2.87 ± 0.57 to 1.65 ± 0.29). Oral administration of GS in a dosage of 26.4 g/kg did not lead to toxic effects in rats.
  
  
  CONCLUSIONS
  GS attenuated the IR injury in the presence of cholestasis and could be considered for the clinical treatment of cholestasis.
authors.affiliation: Zhejiang Chinese Medical Hospital, The First Affiliated Hospital of Zhejiang Chinese Medical University , Hangzhou , China.
authors.forename: Yong-qing
authors.initials: YQ
authors.lastname: Fu
authors.forename: Chen
authors.initials: C
authors.lastname: Hua
authors.forename: Jian
authors.initials: J
authors.lastname: Zhou
authors.forename: Bing-rong
authors.initials: BR
authors.lastname: Cheng
authors.forename: Jun
authors.initials: J
authors.lastname: Zhang
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D004195:Disease Models, Animal; D018056:Hemorheology; D020287:In Situ Nick-End Labeling; D041781:Jaundice, Obstructive / Q000150:complications / Q000188:drug therapy* / Q000473:pathology; D008099:Liver / Q000098:blood supply* / Q000187:drug effects / Q000473:pathology; D008111:Liver Function Tests; D051379:Mice; D008813:Mice, Inbred ICR; D005894:Panax / Q000737:chemistry*; D018517:Plant Roots / Q000737:chemistry; D020011:Protective Agents / Q000302:isolation & purification / Q000627:therapeutic use* / Q000633:toxicity; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D012503:Saponins / Q000302:isolation & purification / Q000627:therapeutic use* / Q000633:toxicity
chemical_list: D020011:Protective Agents; D012503:Saponins