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Aim: To investigate the chemical constituents of the rhizomes of Dioscorea panthaica Prain et Burkill and look for new active compounds., Methods: The compounds were isolated with silica gel and HPLC, and their structures were elucidated on the basis of chemical evidences and spectral analysis (IR, ESI-MS, 1HNMR, 13CNMR, DEPT, 1H-1H COSY, HMQC, HMBC, NOESY)., Results: Three steroidal saponins were isolated from the rhizomes of Dioscorea panthaica. They were elucidated as 26-O-beta-D-glucopyranosyl-3 beta, 26-diol-23(S)-methoxy-25(R)-delta 5,20(22)-diene-furosta-3-O-[alpha-L-rhamnopyranosyl-(1-->2)- O-alpha-L-rhamnopyranosyl-(1-->4)]-beta-D-glucopyranoside (I), pseudoprotodioscin (II), 26-O-beta-D-glucopyranosyl-3 beta, 26-diol-25 (R)-delta 5,20(22)-diene-furosta-3-O-alpha-L-rhamnopyranosyl- (1-->2)-O-beta-D-glucopyranoside (III)., Conclusion: Compound I is a new steroidal saponin and was named as dioscoreside C. Compound II and III were obtained from this genus for the first time.

The ginseng polysaccharides GH1 (100, 200 mg.kg-1) iv reduced liver glycogen and increased adenosine-3',5'-cyclic monophosphate (cAMP) level and adenyl cyclase (AC) activity in mice. The action of GH1 was completely antagonized by propranolol, inhibitor of adrenergic beta receptor. The stimulating effect of GH1 on AC activity was significant 2 and 4 h after iv GH1. However, GH1 at concentration of 20-120 mumol.L-1 in vitro showed no manifest effect on AC activity. GH1 stimulated the activities of 3',5'-cyclic-GMP phosphodiesterases (PDE) and calmodulin (CaM) in a dose-dependent manner. It is suggested that the reduction of liver glycogen induced by GH1 resulted from its obvious increase of cAMP which promoted glycogenolysis and decreased glycogenesis.

Ginseng polysaccharides (GH1) 50-200 mg/kg ip or sc reduced blood glucose and liver glycogen of mice. Adrenalectomy did not affect this action. GH1 increased the content of pyruvic acid, but decreased the content of lactic acid by weakening the activity of lactate dehydrogenase. GH1 accelerated oxidative-phosphorylation of carbohydrate since the activities of succinate dehydrogenase (SDH) and cytochrome oxidase (CCO) were obviously stimulated. Besides the promotion of the activity of SDH in human embryonic lung fibroblasts (HELF), GH1 decreased the content of polysaccharides in HELF of the 24th age generation, but increased that of the 40th age generation. On the other hand, GH1 stimulated the release of insulin. It is suggested that the reduction of blood glucose and liver glycogen induced by GH1 be primarily due to the increase of carbohydrate utilization and the decrease of glycogenesis.

Ginseng polypeptide (GPP) isolated from the root of Panax ginseng C. A. Meyer was demonstrated to decrease the levels of blood sugar and liver glycogen when injected intravenously to rats at doses of 50-200 mg/kg without affecting total blood lipid. when mice were injected subcutaneously daily at doses of 50 and 100 mg/kg for 7 successive days, GPP was also found to decrease blood glucose and liver glycogen. In addition, GPP was found to decrease various experimental hyperglycemia induced by injection of adrenaline, glucose and alloxan. However, GPP exhibited inhibiting effect on the glycogen enhancement induced by glucose, but strengthening effect on the glycogen decrease induced by adrenaline. When the levels of blood total lipid and liver glycogen were increased by alloxan, GPP was shown to inhibit these changes except its lowering of blood sugar. The toxicity of GPP is very low, its iv LD50 for mice was found to be 1.62 +/- 0.130 g/kg.

When ginseng polypeptide (GP) was administered iv or sc to mice or rats, the blood sugar and liver glycogen were decreased. The decrease of blood sugar and liver glycogen induced by GP in rats were inhibited by pretreatments with pentolamine and propranolol, respectively. The results suggest that the effect of GP on glucose metabolism may be related to adrenergic receptors. In addition, GP at doses which cause decreases of blood sugar and glycogen, inhibited LDH activity, and consequently produced decrease of lactic acid and increase of pyruvic acid. GP was also found to stimulate SDH and CCO activities (which are respiratory enzymes in the electron transport chain), consequently promote aerobic oxidation course.