ETAS®50 Attenuates Ultraviolet-B-Induced Interleukin-6 Expression by Suppressing Akt Phosphorylation in Normal Human Dermal Fibroblasts

Ken Shirato; Tomoko Koda; Jun Takanari; Junetsu Ogasawara; Takuya Sakurai; Hideki Ohno; Takako Kizaki

doi:10.1155/2018/1547120

ETAS®50 Attenuates Ultraviolet-B-Induced Interleukin-6 Expression by Suppressing Akt Phosphorylation in Normal Human Dermal Fibroblasts

Evid Based Complement Alternat Med. 2018 Jul 5:2018:1547120. doi: 10.1155/2018/1547120. eCollection 2018.

Authors

Ken Shirato¹, Tomoko Koda², Jun Takanari³, Junetsu Ogasawara⁴, Takuya Sakurai¹, Hideki Ohno⁵, Takako Kizaki¹

Affiliations

¹ Department of Molecular Predictive Medicine and Sport Science, Kyorin University School of Medicine, 6-20-2 Shinkawa, Mitaka, Tokyo 181-8611, Japan.
² Faculty of Nursing, Tokyo Healthcare University, 2-5-1 Higashigaoka, Meguro, Tokyo 152-8558, Japan.
³ Amino Up Chemical Co. Ltd., 363-32 Shin-ei, Kiyota, Sapporo, Hokkaido 004-0839, Japan.
⁴ Department of Health Science, Asahikawa Medical University, 2-1-1-1 Midorigaoka-Higashi, Asahikawa, Hokkaido 078-8510, Japan.
⁵ Social Medical Corporation, The Yamatokai Foundation, 1-13-12 Nangai, Higashiyamato, Tokyo 207-0014, Japan.

Abstract

We recently reported that ETAS 50, a standardized extract from the Asparagus officinalis stem, exerted anti-inflammatory effects on ultraviolet-B- (UV-B-) irradiated normal human dermal fibroblasts (NHDFs) by inhibiting nuclear factor-κB p65 nuclear import and the resulting interleukin-1β (IL-1β) expression. To further elucidate the antiphotoaging potency of ETAS 50, we examined the anti-inflammatory effects on UV-B-irradiated NHDFs by focusing on the stress-activated mitogen-activated protein kinase (MAPK) and Akt signaling pathways. NHDFs were treated with 1 mg/mL of ETAS 50 or dextrin (vehicle control) after UV-B irradiation (20 mJ/cm²) for different time periods. Phosphorylation levels of c-Jun N-terminal kinase (JNK), p38 MAPK, and Akt were analyzed by western blotting. IL-6 mRNA levels were analyzed by real-time polymerase chain reaction. UV-B-irradiated NHDFs showed increased phosphorylation levels of JNK, p38 MAPK, and Akt, as well as increased mRNA levels of IL-6. ETAS 50 treatment after UV-B irradiation suppressed the increased phosphorylation levels of Akt without affecting those of JNK and p38 MAPK. ETAS 50 as well as Akt inhibitor Perifosine repressed UV-B irradiation-induced IL-6 mRNA expression. These results suggest that ETAS 50 treatment represses UV-B irradiation-induced IL-6 expression by suppressing Akt phosphorylation. The present findings demonstrate the potential of ETAS 50 to prevent photoaging by attenuating UV-B irradiation-induced proinflammatory responses in skin fibroblasts.