AIM　To study the pharmacokinetics of 20(R)-ginsenoside Rg3 (GRg3) in human. METHODS　High-performance liquid chromatography-ultraviolet detection method was used in this study. RESULTS　The pharmacokinetics of GRg3 in 14 healthy volunteers were investigated. After a single oral dose of 3.2 mg.kg-1 in 8 male volunteers, the plasma concentration-time course fitted well to a two-compartment open model, with the following pharmacokinetic parameters: Tmax (0.66±0.10) h, Cmax (16±6) ng.mL-1, T1/2α (0.46±0.12) h, T1/2β (4.9±1.1) h, T1/2(Ka) (0.28±0.04) h, AUC0-∞ (77±26) ng.mL-1.h. No kinetic analysis was made after an oral dose of 0.8 mg.kg-1 GRg3 in 6 other volunteers because of the low concentration, but a good correlation between Cmax and dosage of the two groups was found. CONCLUSION The absorption of GRg3 was rapid in man, and its elimination was rapid after oral administration of ginsenoside Rg3. The pharmacokinetic results shows that it exhibited first order kinetic characteristics.

OBJECTIVETo observe the effect of different doses of acetamide on the histopathology in the cerebral cortex of rats with tetramine (TET) poisoning and to provide a basis for the treatment of fluoroacetamide poisoning with acetamide.

METHODSEighty clean Sprague-Dawley rats were randomly divided into five groups: saline control group,dimethylsulfoxide water solution control group,TET poisoning group, acetamide (2.88 g/kg/d) treatment group, and acetamide (5.68 g/kg/d) treatment group, with 16 rats in each group. Rats in the poisoning group and treatment groups were poisoned with TET by intragastric administration after fasting; then, saline was injected intramuscularly into rats of the poisoning group, and different doses of acetamide were injected intramuscularly into rats of treatment groups; the course of treatment was 5 d. At 3 h, 12 h, 48 h, and 7 d after treatment, the cerebral cortex was harvested from rats in each group, and the histopathological changes in the cerebral cortex were evaluated under light and electron microscopes.

RESULTSThe light microscopy showed that the TET poisoning group had hypoxia changes in the cerebral cortex, which worsened over time; the treatment groups had reduced hypoxia changes, and the acetamide (2.88 g/kg/d) treatment group had more reduction than the acetamide (5.68 g/kg/d) treatment group. The electron microscopy showed that the apoptosis of neuronal cells were the main pathological changes in the TET poisoning group; the treatment groups had reduced apoptotic changes, and the acetamide (2.88 g/kg/d) treatment group had more reduction than the acetamide (5.68 g/kg/d) treatment group.

CONCLUSIONNo pathological changes associated with the synergistic toxic effect of acetamide and TET are found in the cerebral cortex. Acetamide (2.88 g/kg/d) could reduce central nervous lesions, but the efficacy is not improved after increasing the dose. For patients who cannot be identified with TET or fluoroacetamide poisoning, acetamide could be considered for treatment.

Acetamides ; pharmacology ; Animals ; Bridged-Ring Compounds ; toxicity ; Cerebral Cortex ; drug effects ; pathology ; Disease Models, Animal ; Male ; Rats ; Rats, Sprague-Dawley