14.8. IMPROVEMENT OF SEXUAL FUNCTION BY WOLFBERRY
Wolfberry has been used traditionally to enhance sexual function, and there is some scientific evidence for such a claim. In cultured seminiferous epithelium, ultraviolet light-induced lipid peroxidation was inhibited by LBP (Wang et al. 2002). This could indicate an antioxidative ability of LBP; however, ultraviolet exposure does not represent a direct causal factor for declined sex function or fertility. To this effect, hyperthermia is an important risk factor, as seminiferous epithelium is very sensitive to heat. A finding of interest is that hyperthermia-induced structural and functional damage was largely prevented by LBP (Wang et al. 2002; Luo et al. 2006) in vivo. Moreover, free radical-induced cytochrome creduction and H2O2-induced DNA oxidative damage in seminiferous epithelial cells were also inhibited by polysaccharides derived from wolfberry (Wang et al. 2002; Luo et al. 2006). In vivo experiments repeated the effect of LBP on heat-induced functional and structural damage to the testis (Luo et al. 2006). Furthermore, in rats with unilateral castration, LBP improved copulatory performance and reproductive function, such as shortened penis erection latency and mount latency, increased sexual hormone levels, augmented accessory sexual organ weights, and improved sperm quantity and quality (Luo et al. 2006).
As far as the mechanism is concerned, improvement in sexual function by wolfberry is largely linked to its effect on the NO-cGMP axis by providing more substrate for NO synthesis and scavenging ROS (Figure 14.9). In a different experiment, an herbal formulation containing wolfberry seeds enhanced intracavernous pressure and NO-cGMP activity in the penile tissues of male rats (Sohn et al. 2008). Thus, the mechanism of sexual function improvement is unlike that of other erectile enhancement drugs such as sidlenafil, which are potent and selective inhibitors of cGMP-specific phosphodiesterase (PDE) type 5 (PDE5). Wolfberry is suggested to independently augment NO-cGMP bioavailability via PDE.
