Protective effect of ginseng polysaccharides on influenza viral infection.

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.

Antithrombotic and antiplatelet activities of Korean red ginseng extract.

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 concentration-dependent manner, with IC(50) values of 390 +/- 15, 485 +/- 19, 387 +/- 11 and 335 +/- 15 microg/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.

Antiplatelet and antithrombotic activities of Korean Red Ginseng.

The antiplatelet and antithrombotic activities of Korean Red Ginseng (KRG) were examined on rat carotid artery thrombosis in vivo, and platelet aggregation in vitro and ex vivo. Administration of KRG to rats not only prevented carotid artery thrombosis in vivo in a dose-dependent manner, but also significantly inhibited ADP- and collagen-induced platelet aggregation ex vivo, while failed to prolong coagulation times such as activated partial thromboplastin time (APTT) and prothrombin time (PT), indicating the antithrombotic effect of KRG might be due to its antiplatelet aggregation rather than anticoagulation effect. In line with the above observations, KRG inhibited U46619-, arachidonic acid-, collagen- and thrombin-induced rabbit platelet aggregation in vitro in a concentration-dependent manner, with IC50 values of 620 +/- 12, 823 +/- 22, 722 + 21 and 650 +/- 14 microg/mL, respectively. Accordingly, KRG also inhibited various agonists-induced platelet serotonin secretions as it suppressed platelet aggregation. These results suggest that KRG has a potent antithrombotic effect in vivo, which may be due to antiplatelet rather than anticoagulation activity, and KRG intake may be beneficial to the individuals with high risks of thrombotic and cardiovascular diseases.

Panax ginseng improves survival and sperm quality in guinea pigs exposed to 2,3,7,8-tetrachlorodibenzo- p-dioxin.

OBJECTIVES: To further assess the effect of Panax ginseng on survival and sperm quality of guinea pigs exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). MATERIALS AND METHODS: Eighty male guinea pigs were divided into eight equal groups. The normal control (NC) group received vehicle and saline; one dose of 1 micro g/kg body weight TCDD was injected intraperitoneally into the single TCDD-treated (TT) and test groups (P100, P200, C100, C200); G and NC groups received vehicle instead of TCDD. P. ginseng water extract (PG-WE) was injected intraperitoneally at daily doses of 100 (G100, P100, C100) or 200 mg/kg body weight (G200, P200, C200). The PG-WE was 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. RESULTS: All TT animals died within 18 days after TCDD exposure, but 40-70% of the PG-WE-treated groups, depending on the group, survived until death at 40 weeks. All the surviving males were fertile regardless of TCDD exposure; there was no difference in litter size between the NC and test groups. Notably the death rate of progeny born to PG-WE-treated groups was lower than that of progeny born to the NC group. The progeny born to TCDD-exposed groups (P200 and C groups) had a preponderance of females. G Group animals had higher sperm quality than that of NCs even long after discontinuing PG-WE. CONCLUSION: P. ginseng improves the survival rate and sperm quality in guinea pigs exposed to TCDD.

Two-phase partition chromatography using soybean oil eliminates pesticide residues in aqueous ginseng extract.

This study was carried out to develop a cost-, labor- and efficiency-effective elimination method of pesticide residues in ginseng extract. A two-phase partition method between soybean oil and distilled water or aqueous ginseng extract was employed for the elimination of pesticide residues. Content of the pesticides was determined by gas chromatography with electron capture or nitrogen phosphorus detector. A total of 15 pesticides representing four categories (organochlorine, organophosphorus, carbamate, pyrethroid) were spiked (ca. 2 ppm) to 2 ml soybean oil in a test tube and the oil was mixed with 6 ml distilled water or 10% aqueous ginseng extract. The test tubes were then vortexed (2 min) and centrifuged at 3000 rpm for 15 min to separate the oil and aqueous layers. Each layer was harvested and subjected to quantitative analysis of pesticides. The average distribution ratio of the pesticides to the oil layer was 94.4 +/- 6.7% in the mixture of the oil and distilled water, and 105.5 +/- 6.6% in the mixture of the oil and ginseng extract. No significant qualitative and quantitative change of ginsenosides, the active ingredients of Panax ginseng, was observed in the ginseng extract before and after the oil treatment. These results suggest that two-phase partition chromatography between soybean oil and the aqueous phase is a cost-, labor- and efficiency-effective reliable method for the elimination of pesticide residues in ginseng extract.

In vivo effects of Panax ginseng extracts on the cytochrome P450-dependent monooxygenase system in the liver of 2,3,7,8-tetrachlorodibenzo-p-dioxin-exposed guinea pig.

The effects of the subchronic administration of Panax ginseng extracts were examined on the hepatic cytochrome P450-dependent monooxygenase system of guinea pigs pre-exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Panax ginseng extracts were intraperitoneally administered to guinea pigs at 100 mg/kg/day for 14 days from 1 week after a single intraperitoneal injection of 1 microg of TCDD/kg of body weight. TCDD treatment increased the total cytochrome P450 content 2.86-fold, and this was remarkably inhibited by the administration of Panax ginseng extracts. Treatment with ginseng extract alone also decreased the contents of cytochrome P450 by 33%, but both TCDD and ginseng extracts had no effect on cytochrome b(5) content. The administration of TCDD resulted in a 1.73-fold increase in microsomal NADPH-cytochrome P450 reductase activity in the guinea pig liver, and this was significantly inhibited by ginseng extracts, but treatment with ginseng extracts alone had no effect on its activity, and no statistical changes in the activity of NADPH-cytochrome b(5) reductase were observed in guinea pig liver due to TCDD and/or ginseng extract administration. Compared to the control, ECOD activity remarkably (1.76-fold) increased after TCDD administration, but this increase was completely inhibited by treatment with ginseng extract. Treatment with ginseng extract alone resulted in a 50% reduction of ECOD activity. TCDD administration remarkably induced benzphetamine demethylation (BPDM) activity, while ginseng extract also slightly increased the enzyme's activity, but the induction attributed to ginseng extracts was not statistically significant. Even though administration of ginseng extracts slightly inhibited TCDD-induced BPDM activity, the inhibition was not statistically significant. These results indicate that ginseng extract exerts different effect on the induction of P450 isozymes. From these results, we suggest that Panax ginseng extracts may act as an inhibitor of CYP1A rather than that of CYP2B.

Inhibitory effect of tumor cell proliferation and induction of G2/M cell cycle arrest by panaxytriol.

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.