Medical Attributes of Panax spp. - Ginseng

by Paul Downton, Lisa A. Niewinski, and John Telechowski
Wilkes University
Wilkes-Barre, PA

July, 1997

Panax, commonly referred to as ginseng, is a genus of perennial herbs in the Araliaceae (ginseng family). Three species in this genus include Panax quinquefolium, Panax notaginseng, and Panax ginseng. Panax quinquefolium (American or white ginseng) is commonly found in rich woods from Maine to Georgia and from Oklahoma to Minnesota (Foster, 1990). Panax ginseng (Chinese or red ginseng) has been cultivated for thousands of years throughout China, Korea, and Japan (Anon., 1997).

The botanical name Panax is derived from the Greek word for panacea. Ginseng literally means "root of man," because the root of this plant often resembles the shape of a human body (Mindell 1992). The root of Panax species is used medicinally. It takes four to five years before the root has matured enough so that it becomes medically active and worth harvesting. Cultivated varieties deteriorate badly after growing about ten years, whereas the wild root improves with age. Therefore, it is the wild root that is preferred over the cultivated varieties (Anon., 1997).

The root of the Panax species contains saponin glycosides called ginsenosides. Saponin glycosides consist of a sugar residue glycone that is attached to an aglycone saponin. A few of the saponin glocosides isolated from Panax include Rf, Rb1, Rg1, Rg2, and Re. Some of the medical benefits of the ginsenosides include calcium channel blocker functions, prevention of memory loss, anti-tumor activity, anti-coagulant activity, psychotropic activity, ability to lower cholesterol levels, the promotion of immune system functions, and anti-inflammatory effects (Fulder). Conversely, Panax also exhibits negative effects such as inducing allergic reactions and causing hypertension (Mindell, 1992).

The ginsenoside Rf, a saponin present in ginseng, inhibits high threshold voltage dependent calcium channels in rat sensory neurons in the same fashion as a maximal dose of opiods. The influence of Rf is dose dependent, and can be suppressed by pretreatment of neurons with pertussis toxin (Seung-Yeol et al., 1995). Also, the saponins of Panax quinquefolium block the calcium channel on smooth vascular muscle by inhibiting calcium influx through the potential dependent calcium channel and the receptor operated calcium channel (Wu et al., 1995). Rf or related saponins may be suitable for constructing additional modulators of neuronal calcium channels (Seung-Yeul et al., 1995).

The ginsenoside Rb1 has been shown to prevent memory loss in rats caused by a cholinergic agent. Rb1 has been shown to facilitate the release of acetylcholine from hippocampal slices. This causes an increased uptake of choline to the nerve endings helping to prevent memory loss (Benishin et al., 1991).

Anti-tumor polyacetylenes derived from the callus of red ginseng have been shown to inhibit the growth of several cancerous cell lines (Matsunaga et al., 1989). Two polyacetylenes that were isolated exhibited growth inhibition against Yoshida sarcoma cells in tissue culture (Fujimoto and Satoh, 1987). Also two new C17-polyacetylenes and C14-polyacetylene have been isolated from P. quinquefolium (white ginseng). These polyacetylenes all showed some degree of cytotoxicity against leukemia cells. However, the C17-polyacetylenes were shown to be approximately 20 times more effective than the C14-polyacetylenes in their activity against leukemia cells (Fujimoto et al., 1992).

The ginsenoside Rg2 strongly inhibits platelet aggregation caused by three aggregating agents: endotoxin, collagen, and arachidonic acid (Matsuda et al., 1986). Also, 70 percent methanolic extract of red ginseng (RMe) was shown to increase tissue blood flow in rats. RMe inhibited blood coagulation and promoted fibrinolysis. The effects of the 70 percent red methanolic extract were shown to be much stronger than those of the 70 percent white methanolic extract (Matsuda, 1987a).

Crude ginseng saponins and Rb1 isolated from P. ginseng have been shown to have psychotropic effects in mice. The Rb1 and the crude ginseng saponins were shown to be able to decrease antagonistic behavior in mice. Their effects on behavior occurred in a dose dependent manner. However, Rg1 ginsenosides obtained from P. ginseng were not shown to have the same effects (Etou, 1988).

Saponins from P. ginseng have been shown to reduce cholesterol levels in rats. The purified ginsenosides Rb1, Rb2, Re, and Rg1 all appear to have hypocholesterolenic properties. This action is thought to be brought on by an increase of the LDL receptor (Lee et al., 1987).

Seventy percent methanolic extract of P. ginseng (RMe) has been shown to increase phagocytic activity of the mouse reticuloendothelial system. Oral administration of RMe in mice was shown to significantly increase the phagocytic index. RMe was shown to increase lysosomal enzyme activity and the number of peritoneal macrophage cells in mice. RMe also promoted the phagocytosis of latex by peritoneal and pulmonary macrophage cells in vitro. This suggests that RMe is responsible for promoting the phagocytic activity of the reticuloendothelial system (Matsuda et al., 1987b).

Saponins of P. notaginseng were shown to have anti-inflammatory effects. The anti-inflammatory effects were shown to reduce capillary permeability and the inflammatory edema of ear in mice. Carrageenin induced edema of hind paws in rats was also inhibited by P. notaginseng saponins. P. notaginseng saponins showed both direct and indirect anti-inflammatory effects (Hao and Yang, 1986). Also, 20s which was obtained from P. ginseng prevented increases in dermal blood flow, in the shoulder and lumbar regions, that was brought on by stress (Hata et al., 1985).

Along with the medicinal benefits, the Panax species can also induce negative effects. For example, it has been shown to cause hypertension (Mindell, 1992). Furthermore, the P. ginseng has been shown to contain three polyacetylenic sensitizers, including falcarinol and didehydrofalcarinol. Even in low concentrations, such as 0.03%, falcarinol is able to elicit strong allergic reactions. Indeed, the scientist conducting this study himself became sensitized to the Panax ginseng (Hausen et al., 1987).

 

LITERATURE CITED

Anonymous. 1997. NatureÕs Field. http://www.herbalherbal.com/ginseng/html/medical.html

Benishin, C.G., R. Lee, L.C.H. Wang, and A.J. Liu. 1991. Effects of ginsenoside Rb1 on central cholinergic metabolism. Pharmacology 42: 223-229.

Fujimoto, Y. and M. Satoh. 1987. Acetylenes from the callus of Panax ginseng. Phytochemistry (OXF) 26: 2850-2852.

Fujimoto, Y., H. Wang, K. Makoto, M. Satoh, and N. Takeuchi. 1992. Phytochemistry (OXF) 31: 3499-3501.

Fulder, S. 1997. How Ginseng is Used. http://www.herbalherbal.com/ginseng/html/howuse.html

Hao, C.Q. and F. Yang. 1986. Acta Pharmacol Sin 7: 252-255.

Hata, T., T. Kita, K. Atsufum, E. Itoh and Y. Kawashima. 1985. Pharmacobio-DYN 8:1068-1072.

Hausen, B.M., J. Brohan, W.A. Koenig, H. Faasch, H. Hahn, and G. Bruhn. 1987. Allergic and irritant contact dermatitis from falcarinol and didehydrofalcarinol in common ivy. Contact Dermatitis 17: 1-9.

Lee, Y.W., J.H. Koo and C.N. Joo. 1987. Biosynthesis of low density lipoprotein receptor: Effect of ginsenosides on the inhibitor of low density lipoprotein receptor biosynthesis. Korean Biochemical Journal 20: 362-367.

Matsuda, H., K. Namba, S. Fukuda, T. Tani, and M. Kuloo. 1986. Chemical Pharmacological Bulletin (Tokyo) 34: 1153-1157.

Matsuda, H., M. Kubo and M. Mizuno. 1987a. Pharmalogical study on P. ginseng C.A. Meyer: Cardiovascular effect of red ginseng and white ginseng. Shoyakugaku Zasshi 41: 125-134.

Matsuda, H., M. Kubo, T. Tani, I. Kitagawa and M. Mizuno. 1987b. Pharmalogical study on P. ginseng C.A. Meyer: Protective effect of red ginseng on infection: (2). On phagocytic activity of mouse RES. Shoyakugaku Zasshi 41: 135-141.

Matsunaga, H., M. Katano, H. Yamamoto, M. Mori and K. Takata. 1989. Studies on the panarytriol of Panax ginseng C.A. Meyer: Isolation, determination and anti-tumor activity. Chemical Pharmaceutical Bulletin 37(5): 1279-1281.

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Seung-Yeol, N., H.J. Park and E. W. McClesky. 1995. A trace component of ginseng that inhibits Ca2+ channels through a pertussis toxin-sensitive G protein. Proceedings of the National Acadamy of Sciences of the United States, 92: 8739.

Wu, J., X.J. Yu, and C.H. Liu. 1995. Effects of saponins of Panax quinquefolium leaf and stem on isolated rabbit aortic strips. Zhongguo Yaolixue Yu Dulixue Zazh 9(2):155-156.

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This paper was developed as part of the BIO 368 - Medical Botany course offered at Wilkes University during the summer of 1997. Course instructor was Kenneth M. Klemow, Ph.D. (kklemow@wilkes.edu). The information contained herein is based on published sources, and is made available for academic purposes only. No warrantees, expressed or implied, are made about the medical usefulness or dangers associated with the plant species in question.

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This page posted and maintained by Kenneth M. Klemow, Ph.D., Biology Department, Wilkes University, Wilkes-Barre, PA 18766. (570) 408-4758, kklemow@wilkes.edu.