Biological and Pharmaceutical Bulletin · 2004 · 61 citations · 16 references
MedicineMedicinal ChemistryPharmacologyBiochemical PharmacologyClinical PharmacologyInflammationAnti-inflammatory PharmacologyNeuroprotectionNeuroprotective PharmacologyAntioxidant TreatmentCerebral Ischemia NeuroprotectionCerebral Ischemia Reperfusion InjuryIschemic Injury ResponseIschemic Organ InjuryLipopolysaccharide BiosynthesisProstaglandin Synthesis InhibitionRodent Cerebral Ischemia
Ginseng was incubated under mildly acidic conditions and its inhibitory effect on a rat ischemia-reperfusion model was investigated. When ginseng was treated with 0.1% hydrochloric acid at 60 degrees C, its protopanaxadiol saponins were transformed to diasteromeric ginsenoside Rg3 and Delta20-ginsenoside Rg3. When the transformed ginseng extract, of which the main component was ginsenosides Rg3, was treated with human intestinal microflora, the main metabolite was ginsenoside Rh2. Orally administered acid-treated ginseng (AG) extract and ginsenoside Rh2 potently protect ischemia-reperfusion brain injury. The ginsenoside Rh2 also inhibited prostaglandin-E2 synthesis in lipopolysaccharide-stimulated RAW264.7 cells, but showed no in vitro antioxidant activity. These results suggest that AG and ginsenoside Rh2 can improve ischemic brain injury.
16
Teruaki Akao, Hiroaki Kida, Matao Kanaoka et al. · Journal of Pharmacy and Pharmacology · 1998 · 276 citations