This study was conducted to investigate whether and how Jumihaidokuto (JHT), a traditional Chinese medicine, prevents UVB-induced skin damage in male HR-1 hairless mice. JHT has been traditionally prescribed for patients presenting skin disorders with redness and swelling, and, in Japan, it is approved for prescription to patients with acute and/or purulent skin disorders, hives, acute eczema, and athlete’s foot. Considering the traditional use of JHT, we hypothesized that oral administration of JHT might emerge as an effective strategy to prevent UVB-induced skin damage, such as edema and erythema. Here, we pretreated mice with JHT (1000 mg/kg, p.o.) for 3 weeks and then administered a single dose of UVB irradiation (250 mJ/cm2) on the dorsal skin. UVB irradiation increased the erythema index and transepidermal water loss (TEWL) and decreased the skin water content in the epidermis at 72 h post-irradiation. JHT treatment inhibited the increase of TEWL and the loss of water content in the epidermis, but not the elevation of the erythema index. Moreover, administration of JHT suppressed UVB-induced epidermal hyperplasia by blocking the proliferation of keratinocytes and also inhibited irradiation-triggered reduction of collagen fibers and infiltration of immune cells into the dermis. Lastly, administration of JHT suppressed UVB-induced production of proinflammatory mediators, such as prostaglandin E2 and interleukin-1β. These results suggest that JHT prevents UVB-induced skin damage and that the underlying mechanism involves the inhibition of proinflammatory mediators.

Yokukansankachimpihange (YKSCH), a traditional Japanese medicine composed of 9 crude drugs, is designed to improve neurosis, insomnia in adults, and night crying in children. YKSCH has been reported to improve diurnal rhythm in patients with Alzheimer's disease and prolong the total sleeping time in healthy subjects. However, little is known about how YKSCH alleviates sleep disorders. Here, we investigated whether and how YKSCH treatment affected sleep latency and duration in group-housed and socially isolated mice. Male ddy mice were treated with YKSCH [1,500 mg/kg, per os (p.o.)] in group-housed or socially isolated conditions for 3-4 weeks. After the last injection, mice were intraperitoneally (i.p.) administered with pentobarbital (60 mg/kg) and the sleep latency and duration was evaluated. The results show that pretreatment with YKSCH had no effect on sleep latency or duration in group-housed mice. However, YKSCH treatment significantly improved the reduced sleep duration in socially isolated mice. This effect of YKSCH was inhibited by the administration of bicuculline (3 mg/kg, i.p.), a GABA A receptor antagonist. Furthermore, we showed that YKSCH treatment improved the decrease in allopregnanolone content and its synthase expression levels in the olfactory bulb. These results suggest that YKSCH treatment improved social isolation stress-induced insomnia via the GABAergic pathway and that the mechanism of action of YKSCH is partly due to improvement of allopregnanolone levels of expression.

A single high-dose ultraviolet B (UVB) exposure on the skin induces acute inflammatory responses, such as an increase in proinflammatory cytokines (e.g., IL-6 and IL-1β), hyperpermeability and dilation of blood and lymphatic vessels, and infiltration of inflammatory cells. These responses result in different cutaneous disorders characterized by erythema, epidermal hyperplasia, edema formation, and extracellular matrix degradation. Saireito extract (SRT), a traditional Chinese medicine, has been used to treat various inflammatory diseases in Japan, and SRT and its major active components (e.g., saikosaponins and baicalin) were reported to downregulate proinflammatory cytokines. Moreover, SRT has a protective effect against UV irradiation in vitro. Based on these findings, we aimed to investigate the effect of SRT on UVB-induced photodamage and structural change in the vasculature. We pretreated male HR-1 hairless mice with SRT (625 or 1250 mg/kg) for 3 weeks before a single UVB (250 mJ/cm2) irradiation. SRT treatment attenuated UVB-induced increases in erythema, transepidermal water loss, and edema formation at 72 h after irradiation. SRT treatment also suppressed UVB-induced inflammatory cell infiltration and collagen degradation. Furthermore, at 24 h after irradiation, SRT treatment inhibited UVB-induced upregulation of proinflammatory cytokines and reduction in lymphatic vessel density associated with upregulation of VEGF-C expression. These results suggest that SRT could attenuate UVB-induced photodamage. This protective effect of SRT involves suppression of upregulation of proinflammatory cytokines and improvement of lymphatic function in the early stage of inflammation.