Oral administration of Jumihaidokuto inhibits UVB-induced skin damage and prostaglandin E2 production in HR-1 hairless m
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ORIGINAL PAPER
Oral administration of Jumihaidokuto inhibits UVB‑induced skin damage and prostaglandin E2 production in HR‑1 hairless mice Kenta Murata1 · Manami Oyama1 · Misaki Ogata1 · Nina Fujita1 · Ryuji Takahashi1 Received: 4 June 2020 / Accepted: 2 November 2020 © The Author(s) 2020
Abstract 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. Keywords Jumihaidokuto · UVB · Collagen · Elastin · Prostaglandin E2
Introduction The ultraviolet (UV) light that reaches the earth’s surface is composed of 90% UVA (320–400 nm) and 10% UVB (280–320 nm). Acute exposure of the skin to UVB produces various harmful effects, including inflammation, impaired skin barrier function, photoaging, and carcinogenesis. Skin inflammation is characterized by erythema, swelling, edema, and itching. In UVB-induced skin inflammation, oxidative stress plays a pivotal role in initiating and driving the cellular response to UVB irradiation [1] and enhances the production of diverse proinflammatory mediators, such as prostaglandin (PG) E2 [2], a key signaling molecule in UVB-induced inflammation. PGE2, the most abundant PG in humans, is generated by the action of cyclooxygenase (COX) enzymes * Ryuji Takahashi [email protected] 1
Kampo Research Laboratories, Kracie Pharma, Ltd., 3‑1 Kanebo‑machi, Takaoka, Toyama 933‑0856, Japan
and plays a crucial role in initiating various aspects of the inflammatory response. For example, PGE2 increases vascular permeability in blood vessels to facilitate the infiltration o
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