Introduction Many menopausal women experience climacteric symptoms including impairment of sexual function. Recent reports have suggested that Korean red ginseng (KRG) has a relaxing effect on the clitoral cavernosal muscle and vaginal smooth muscle in rats. Aim We assessed whether KRG extracts would improve sexual function in menopausal women. Methods Thirty-two menopausal women participated in a placebo-controlled, double-blind, crossover clinical study with administration of either three capsules of ginseng (1 g per capsule) or placebo daily. After completing the KRG or placebo arm, the participants were crossed over to the other arm after a 2-week washout period. The efficacy and safety of the KRG extracts were measured by using questionnaires. Main Outcome Measures Female Sexual Function Index (FSFI) and Global Assessment Questionnaire (GAQ). Results Twenty-eight women completed the study. They were, on average, 51.2 ± 4.1 years old, and their mean menopausal state was for a duration of 37.4 ± 2.9 months. Few carryover effects were noted in either study arm. The ginseng extract significantly improved scores on the FSFI from 3.10 ± 0.87 to 3.50 ± 0.72 in the sexual arousal domain (P = 0.006). The GAQ was more significantly affected by ginseng extracts than by placebo (P = 0.046). There were no severe adverse events in the KRG group, although two cases of vaginal bleeding occurred during KRG treatment. Conclusions Oral administration of KRG extracts improved sexual arousal in menopausal women. Red ginseng extracts might be used as an alternative medicine in menopausal women to improve their sexual life.

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The triterpene saponin ginsenoside Rh2 has been shown to have antiproliferative effects on various cancer cells. However, the effect of Rh2 on the cell cycle and its underlying molecular mechanism in human leukemia cells are not fully understood. In this study, we found that Rh2 inhibited the proliferation of human leukemia cells concentration- and time-dependently with an IC(50) of ~38 µM. DNA flow cytometric analysis indicated that Rh2 blocked cell cycle progression at the G(1) phase in HL-60 and U937 cells, and this was found to be accompanied by the downregulations of cyclin-dependent kinase (CDK) 4, CDK6, cyclin D1, cyclin D2, cyclin D3 and cyclin E at the protein level. However, CDK inhibitors (CDKIs), such as p21(CIP1/WAF1) and p27(KIP1), were gradually upregulated after Rh2 treatment at the protein and messenger RNA (mRNA) levels. In addition, Rh2 markedly enhanced the bindings of p21(CIP1/WAF1) and p27(KIP1) to CDK2, CDK4 and CDK6, and these bindings reduced CDK2, CDK4 and CDK6 activities. Furthermore, Rh2 induced the differentiation of HL-60 cells as demonstrated by biochemical assays and the expression levels of cell surface antigens. In addition, treatment of HL-60 cells with Rh2 significantly increased transforming growth factor-β (TGF-β) production, and cotreatment with TGF-β neutralizing antibody prevented the Rh2-induced downregulations of CDK4 and CDK6, upregulations of p21(CIP1/WAF1) and p27(KIP1) levels and the induction of differentiation. These results demonstrate that the Rh2-mediated G(1) arrest and the differentiation are closely linked to the regulation of TGF-β production in human leukemia cells.

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