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to that of androgenic steroids, being direct action on the syntheses of RNA and protein (Wang et al., 1982).

Ginseng root extract was shewn to stimulate the incorporation of labelled precursors into rat kidney nuclear RNA in a dose dependent manner, maximal effect for incorporation being produced within 8 hrs and and for sequential cytoplasmic RNA synthesis within 10 hrs. The incorporation of leucine into rat renal protein was also increased within 12 hrs of intraperitoneal administration (Nagasawa et al., 1977). Ginseng was shewn to stimulate protein synthesis in human fibroblasts, confirming that constituents of ginseng extract are able to act directly on human cells with resultant accumulation of protein. Ginseng extracts were also capable of inhibiting proteolysis of long-lived proteins in human diploid fibroblasts (Lu and Dice, 1985).

The incorporation of [3H]-uridine into liver and kidney RNA and [3H]-leucine into protein was increased in mice receiving 25 mg/kg total leaf and stem saponins orally daily for 7 days although [3H]-thymidine incorporation was unaltered. In reserpinized animals ginsenosides had no effect on the formation of RNA and protein in liver and kidney (Zhang et al., 1985). Synthesis of DNA in liver and kidney was also unchanged although DNA increased in bone marrow cells (Wen et al., 1982). Bone marrow mitosis was enhanced with resultant increase in the numbers of totally nucleated cells in the bone marrow and of reticulocytes in the peripheral blood (Yamamoto et al., 1977). In further work individual pure ginsenosides Rb2, Rc, Re and Rg1 were administered to rats intraperitoneally at a dose of 5-10 mg/kg with consequent increase in DNA, RNA, protein and formation of lipids in bone marrow cells. Ginsenosides Rb2, Rc and Rg1 caused decreased cAMP (cyclic adenosine monophosphate) and increased cGMP (cyclic guanosine monophosphate) in the bone marrow 20 min after injection (Yamamoto et al., 1978). Such evidence supports the early view of ginseng as an effective tonic.

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