title: Extrusion process of Acanthopanax senticosus leaves enhances the gastroprotective effect of compound 48/80 on acute gastric mucosal lesion in rats.
abstract: OBJECTIVE
  To investigate the gastroprotective effects of Acanthopanax senticosus leaves (ASLs) extrusion on acute gastric mucosal lesion in rats induced by compound 48/80 (C48/80).
  
  
  METHODS
  Rats were divided into six groups: normal; C48/80-induced gastric lesion control; gastric lesion positive control (famotidine 4 mg/kg); gastric lesion administered with two levels of extruded ASLs (ASLE, 40 and 200 mg/kg); and gastric lesion treated with ASLs (ASL 200 mg/kg). Mucus secretion/damage was determined by immunohistological staining. Immunofluorescence and western blotting were performed to determine gastric mucosal Bax and Bcl-2 expression. Gastric mucosal oxidative-stress-related enzymes and malondialdehvde were determined.
  
  
  RESULTS
  C48/80-induced mucus depletion and inflammation in the gastric mucosa were significantly attenuated by ASLs. The increased serum serotonin and histamine concentrations in C48/80-treated rats were also attenuated by ASLs. Gastric mucosal Bax protein expression was increased and Bcl-2 expression was decreased after C48/80 treatment, and ASLs ameliorated Bax and Bcl-2 expression. The extrusion process significantly augmented the effects of ASLs in a dose-dependent manner. ASLEs at 200 mg/kg normalized mucus damage/secretion, C48/80-induced increases of mucosal myeloperoxidase activity (index of inflammation), xanthine oxidase, and malondialdehyde content (index of lipid peroxidation). The effects of ASLs on Bax and Bcl-2 expression were also enhanced by extrusion. Furthermore, these effects of ASLEs at 200 mg/kg were similar to those of famotidine, a histamine H2-receptor antagonist commonly used to treat gastric ulcers.
  
  
  CONCLUSIONS
  ASLEs prevented acute gastric mucosal lesion progression induced by C48/80, possibly by inducing mucus production, and reduced inflammation and oxidative stress in gastric mucosa through an anti-apoptotic mechanism.
authors.forename: Hye Kyung
authors.initials: HK
authors.lastname: Kim
authors.forename: Myung-Gyou
authors.initials: MG
authors.lastname: Kim
authors.forename: Kang-Hyun
authors.initials: KH
authors.lastname: Leem
mesh_terms: D000818:Animals; D004357:Drug Synergism; D004359:Drug Therapy, Combination; D004365:Drugs, Chinese Herbal / Q000008:administration & dosage*; D028001:Eleutherococcus / Q000737:chemistry*; D005753:Gastric Mucosa / Q000187:drug effects / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D006632:Histamine / Q000378:metabolism; D006801:Humans; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018515:Plant Leaves / Q000737:chemistry; D051381:Rats; D017208:Rats, Wistar; D013276:Stomach Ulcer / Q000188:drug therapy / Q000378:metabolism / Q000517:prevention & control*; D014969:Xanthine Oxidase / Q000378:metabolism; D003189:p-Methoxy-N-methylphenethylamine / Q000008:administration & dosage*
chemical_list: D004365:Drugs, Chinese Herbal; D003189:p-Methoxy-N-methylphenethylamine; D008315:Malondialdehyde; D006632:Histamine; D005979:Glutathione Peroxidase; D014969:Xanthine Oxidase