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The roots of Panax ginseng C. A. Meyer, known as Korean ginseng have been a valuable and important folk medicine in the East Asian countries, such as China, Korea and Japan for about 2000 years. Panax is derived from a word “panacea”, which means cure-all diseases and longevity as well as physical strength and resistance. As the use of traditional Chinese herbs as a food supply becomes more and more popular in the western countries, sales of Panax ginseng are increasing in North America and Europe as well as other parts of the world. Active constituents found in most ginseng species include ginsenosides, polysaccharides, peptides, polyacetylenic alcohols and fatty acids. Major active components in Panax ginseng are the ginsenosides, a group of saponins with triterpenoid dammarane structure. More than 30 ginsenosides have been isolated, and known compounds are identified but new compounds were elucidated. Pharmacological effects of ginseng have been demonstrated in cancer, diabetes mellitus, cardiovascular system, immune system and central nervous system including anti-stress and anti-oxidant activity. We have focused this review on the effect of ginseng on diabetes, anticancer activity and cardiovascular system and chemical structures of ginsenosides. In addition, our recent biological study on 20(S)-ginsenoside Rg3 is also touched upon as follows. Multidrug resistance (MDR) has been a major problem in cancer chemotherapy. In this study in vitro and in vivo modulations of MDR by 20(S)-ginsenoside Rg3 (Rg3), a saponin characteristic of red ginseng, was investigated. In flow cytometric analysis using rhodamine 123 as an artificial substrate, Rg3 promoted accumulation of rhodamine 123 in drug-resistant human fibrocarcinoma KBV 20C cells in a dose-dependent manner, but it had no effect on parental KB cells. Additionally Rg3 inhibited [3H]-vinblastine efflux and reversed MDR to DOX (doxorubicin), COL, VCR (vincristine) and VP-16 in KBV20C cells. Reverse transcriptase-polymerase chain reaction and immuno-blot analysis after exposure of KBV20C cells to Rg3 showed that inhibition of drug efflux by Rg3 was due to neither repression of MDR1 gene expression nor P-glycoprotein (Pgp) level. Photo-affinity labeling study with [3H]-azidopine, however, revealed that Rg3 competed with [3H]-azidopine for binding to the Pgp demonstrating that G-Rg3 competed with anticancer drug for binding to Pgp thereby blocking drug efflux. Furthermore, Rg3 increased life span in mice implanted with DOX-resistant murine leukemia P388 cells in vivo and inhibited body weight increase significantly. Further clinical trial of Rg3 in reversal of Pgp-associated MDR is highly feasible.