The nuclear factor-B (NF-B

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.

ABSTRACT

Introduction Aquaporins (AQPs) are membrane proteins that facilitate water movement across biological membranes. There has been little research on the role of AQPs in the female sexual arousal response. Aim The purposes of this study were to investigate the localization and functional roles of AQP1, AQP2, and AQP3 in rat vagina. Methods Female Sprague-Dawley rats (230–240 g, N=20) were anesthetized. The vaginal branch of the pelvic nerve was stimulated for 60 seconds (10 V, 16 Hz, 0.8 ms), and the animals were sacrificed either immediately or 5 minutes later. The expression and cellular localization of AQP1, 2, and 3 were determined by Western blot and immunohistochemistry of the vagina. The intracellular membrane and plasma membrane fractions of the proteins in vaginal tissue were studied by immunoblot analysis with the differential centrifugation. Main Outcome Measures The expression and cellular localization of AQPs, and pelvic nerve stimulation induced translocation of AQPs in rat vaginal tissue. Results Immunolabeling showed that AQP1 was mainly expressed in the capillaries and venules of the vagina. AQP2 was expressed in the cytoplasm of the epithelium, and AQP3 was mainly associated with the plasma membrane of the vaginal epithelium. AQPs were found to be present primarily in the cytosolic fraction of untreated tissues. The translocation of AQP1 and 2 isoforms from the cytosolic compartment to the membrane compartment was observed immediately after nerve stimulation and had declined at 5 minutes after nerve stimulation, while the subcellular localization of AQP3 was not changed by nerve stimulation. Conclusions These results showed a distinct localization of AQPs in the rat vagina. Pelvic nerve stimulation modulated short-term translocation of AQP1 and 2. These results imply that AQPs may play an important role in vaginal lubrication.

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Introduction The expression of aquaporin (AQP) water channels in rat vagina was recently reported. Aim The purposes of this study were to investigate the effect of 17β-estradiol on the expression of the AQP-1 and AQP-2 water channels and nitric oxide synthase (NOS) isoforms in rat vagina. Methods Female Sprague-Dawley rats (230–240 g, N = 90) were divided into three groups: control (N = 30), bilateral ovariectomy (N = 30), and bilateral ovariectomy, followed by subcutaneous injections of 17β-estradiol (50 µg/kg/day, N = 30). After 4 weeks, genital hemodynamics and vaginal secretions were measured after pelvic nerve stimulation, and the animals were then killed. The expression and cellular localization of AQP-1, AQP-2, endothelial NOS (e-NOS), and neuronal NOS (n-NOS) were determined in each group by immunohistochemistry and Western blot. Main Outcome Measures The expression and cellular localization of AQPs and NOS isoforms after estrogen deprivation. Results Estimated vaginal secretions (mg, mean ± standard error) were significantly lower in the ovariectomized group (2.9 ± 0.62) than in the control group (5.7 ± 1.25) and returned to the control value in the group after treatment with 17β-estradiol (6.5 ± 1.22) (P < 0.05). Both AQP-1 and e-NOS immunoreactivities were localized in the capillaries and venules of the lamina propria of the vagina, and n-NOS was expressed in the nerve fibers of the subepithelial lamina propria. The expression of AQP-2 was localized solely in the superficial layer of the vaginal epithelium. The protein expressions of AQP-2, e-NOS, and n-NOS were significantly lower after ovariectomy and were restored to the control level after 17β-estradiol treatment. However, there was no significant change in AQP-1 expression. Conclusions Decreased vaginal secretion after estrogen deprivation may be partly due to functional changes in both AQPs and NOS isoforms in the vagina. The potential role of AQPs in water transport in the vagina might differ according to the type of AQP.

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