title: Oral administration of ginseng ameliorates cyclosporine-induced pancreatic injury in an experimental mouse model.
abstract: BACKGROUND
  This study was performed to investigate whether ginseng has a protective effect in an experimental mouse model of cyclosporine-induced pancreatic injury.
  
  
  METHODS
  Mice were treated with cyclosporine (30 mg/kg/day, subcutaneously) and Korean red ginseng extract (0.2 or 0.4 g/kg/day, oral gavage) for 4 weeks while on a 0.01% salt diet. The effect of ginseng on cyclosporine-induced pancreatic islet dysfunction was investigated by an intraperitoneal glucose tolerance test and measurements of serum insulin level, β cell area, macrophage infiltration, and apoptosis. Using an in vitro model, we further examined the effect of ginseng on a cyclosporine-treated insulin-secreting cell line. Oxidative stress was measured by the concentration of 8-hydroxy-2'-deoxyguanosine in serum, tissue sections, and culture media.
  
  
  RESULTS
  Four weeks of cyclosporine treatment increased blood glucose levels and decreased insulin levels, but cotreatment with ginseng ameliorated the cyclosporine-induced glucose intolerance and hyperglycemia. Pancreatic β cell area was also greater with ginseng cotreatment compared with cyclosporine monotherapy. The production of proinflammatory molecules, such as induced nitric oxide synthase and cytokines, and the level of apoptotic cell death also decreased in pancreatic β cell with ginseng treatment. Consistent with the in vivo results, the in vitro study showed that the addition of ginseng protected against cyclosporine-induced cytotoxicity, inflammation, and apoptotic cell death. These in vivo and in vitro changes were accompanied by decreases in the levels of 8-hydroxy-2'-deoxyguanosine in pancreatic β cell in tissue section, serum, and culture media during cotreatment of ginseng with cyclosporine.
  
  
  CONCLUSIONS
  The results of our in vivo and in vitro studies demonstrate that ginseng has a protective effect against cyclosporine-induced pancreatic β cell injury via reducing oxidative stress.
authors.affiliation: Convergent Research Consortium for Immunologic Disease, The Catholic University of Korea, Seoul, Korea.
authors.forename: Sun Woo
authors.initials: SW
authors.lastname: Lim
authors.forename: Kyoung Chan
authors.initials: KC
authors.lastname: Doh
authors.forename: Long
authors.initials: L
authors.lastname: Jin
authors.forename: Shang Guo
authors.initials: SG
authors.lastname: Piao
authors.forename: Seong Beom
authors.initials: SB
authors.lastname: Heo
authors.forename: Yu Fen
authors.initials: YF
authors.lastname: Zheng
authors.forename: Soo Kyung
authors.initials: SK
authors.lastname: Bae
authors.forename: Byung Ha
authors.initials: BH
authors.lastname: Chung
authors.forename: Chul Woo
authors.initials: CW
authors.lastname: Yang
mesh_terms: D000284:Administration, Oral; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D016572:Cyclosporine / Q000009:adverse effects; D004195:Disease Models, Animal; D050417:Insulin-Secreting Cells / Q000187:drug effects; D007515:Islets of Langerhans / Q000187:drug effects / Q000473:pathology; D007677:Kidney Function Tests; D008264:Macrophages / Q000187:drug effects / Q000473:pathology; D051379:Mice; D009573:Nitrites / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D005894:Panax / Q000737:chemistry*; D010179:Pancreas / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D010182:Pancreatic Diseases / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism*; D010936:Plant Extracts / Q000008:administration & dosage*
chemical_list: D009573:Nitrites; D010936:Plant Extracts; D016572:Cyclosporine