Abstract:The antithrombotic and antiplatelet activities of Korean red ginseng extract (KRGE) were examined on rat carotid artery thrombosis in vivo and platelet aggregation in vitro and ex vivo. The KRGE significantly prevented rat carotid arterial thrombosis in vivo in a dose-dependent manner. Administration of the KRGE to rats significantly inhibited adenosine diphosphate (ADP)-and collagen-induced platelet aggregation ex vivo, although it failed to prolong coagulation times such as activated partial thromboplastin and prothrombin time indicating that the antithrombotic effect of the red ginseng may be due to its antiplatelet aggregation rather than anticoagulation effect. In line with the above observations, the red ginseng inhibited the U46619-, arachidonic acid-, collagen-and thrombin-induced rabbit platelet aggregations in vitro in a concentrationdependent manner, with IC 50 values of 390 ± 15, 485 ± 19, 387 ± 11 and 335 ± 15 µg/ml, respectively. Consistently, serotonin secretion was also inhibited by ginseng in the same pattern. These results suggest that the red ginseng has a potent antithrombotic effect in vivo, which may be due to the antiplatelet rather than the anticoagulation activity, and the red ginseng intake may be beneficial for individuals with high risks of thrombotic and cardiovascular diseases.Platelets not only play a critical role in normal haemostasis, but are also important contributors to thrombotic disorders, especially cerebral vascular diseases such as transient ischaemic attack [1], ischaemic heart diseases such as myocardial infarction [2,3], and peripheral vascular diseases [4]. Disruption of the endothelium by trauma, or atherosclerosis, allows platelets to come into contact with and adhere to exposed subendothelial structures, such as collagen and von Willebrand factor [5][6][7][8] and to interact with soluble agonists, such as ADP and thrombin, both of which were exposed or generated at the injury site [9]. Upon various agonists clustering with respective receptors on platelet surface, the intracellular signals will be activated and platelets will change shape, spread, and release or secrete activating substances to recruit platelets to the developing thrombus. Thus, antiplatelet therapy is a useful means of preventing acute thromboembolic artery occlusions in cardiovascular diseases.Panax ginseng, the herbal root of Panax ginseng C. A. Meyer, has been used for more than 2000 years as a component of traditional Asian medicines to promote health and treat illness. Although various forms of ginseng were processed for use, white ginseng and red ginseng were used most widely. White ginseng is air-dried, while red ginseng is produced by steaming and drying of raw ginseng. It has been reported that red ginseng was pharmacologically more active than white ginseng. The different biological activities of red and white ginsengs may result from production of different chemical constituents during the steaming process. Ginseng saponins, referred to as ginsenosides, are believed to have a ...

Ginseng polysaccharide has been known to have multiple immunomodulatory effects. In this study, we investigated whether Panax ginseng polysaccharide (GP) would have a preventive effect on influenza infection. Administration of mice with GP prior to infection was found to confer a survival benefit against infection with H1N1 (A/PR/8/34) and H3N2 (A/Philippines/82) influenza viruses. Mice infected with the 2009 H1N1 virus suspended in GP solution showed moderately enhanced survival rates and lower levels of lung viral titers and the inflammatory cytokine (IL-6). Daily treatment of vaccinated mice with GP improved their survival against heterosubtypic lethal challenge. This study demonstrates the first evidence that GP can be used as a remedy against influenza viral infection.

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Panaxytriol, a polyacetylenic compound, isolated from red ginseng (Panax ginseng C.A. Meyer), was studied to determine its effects on the growth and cell cycle of tumor cell lines. The compound showed both significant cytotoxicity and inhibition of DNA syntheses in various tumor cells tested. For P388D1, a mouse lymphoma cell line, IC50 values for cytotoxicity and inhibition of DNA synthesis were 3.1 and 0.7 microg/ml, respectively. The cytotoxic effect of panaxytriol was both time- and dose-dependent. It also induced the cell cycle arrest of P388D1 at the G2/M phase, which was measured through flow cytometry. Particularly, the proportion of cells in the G2/M phase of the cell cycle increased from 9 % to 26 and 48 %, respectively, after 24 and 36 h exposure to panaxytriol at 5 microg/ml. There were corresponding decreases in the proportion of cells at the G0/G1 phase. The S phase also decreased during the 36-h treatment.

administered to the P and G groups for 12 weeks from 1 week before TCDD exposure, and to the C groups for 10 weeks from 1 week after TCDD exposure. After a 4-week discontinuation of PG-WE treatment after the 13th week the surviving males were then tested for fertility by mating them with females. The litter size, death rate, male/ female birth ratio and physical abnormalities of the progeny were investigated. After confirming delivery of the offspring, the parent males were killed at 40 weeks, their testes weighed and sperm quality assessed.