Red ginseng extracts attenuate skin inflammation in atopic dermatitis through p70 ribosomal protein S6 kinase activation

Journal of Pharmacological Sciences

Katsuyuki Miura¹  Hiroshi Iwao²  Yasukatsu Izumi³  Keiichi Samukawa³  Shuhei Tomita³  Mayuko Osada-Oka⁴  Yukiko Minamiyama⁴  Sayaka Hirai⁴  Kazuhiro Misumi⁴ 

[1] Applied Pharmacology and Therapeutics, Osaka City University Medical School, Osaka, Japan;Department of Education, Shitennoji University, Habikino, Japan;Department of Pharmacology, Osaka City University Medical School, Osaka, Japan;Food Hygiene and Environmental Health, Division of Applied Life Science, Graduate School of Life and Environmental Sciences, Kyoto Prefectural University, Kyoto, Japan;

关键词: p70 ribosomal protein S6 kinase;    Red ginseng;    Atopic dermatitis;    Basophil;    Keratinocyte;   

DOI  :  10.1016/j.jphs.2017.11.002

来源: DOAJ

【 摘 要 】

Atopic dermatitis (AD) is a chronic and relapsing inflammatory skin disease with increased immunoglobulin E (IgE) levels. Activation of the mammalian target of rapamycin (mTOR)/p70 ribosomal protein S6 kinase (p70S6K) signaling is known to occur in the inflammatory regions of AD skin. We previously demonstrated that red ginseng extract (RGE), as an anti-inflammatory agent, had potential for treating AD. However, it is still unclear whether RGE inhibits mTOR/p70S6K signaling. Thus, we examined the anti-inflammatory effects of RGE on IgE or interferon-γ (IFN-γ) induced signaling pathways. In KU812 human basophils, activation of Fcε receptor type Iα (FCεRI), also known as the high affinity IgE receptor, induced phosphorylation of both mTOR and p70S6K. Moreover, levels of phosphorylated p70S6K (p-p70S6K), but not p-mTOR, were decreased by RGE. RGE also decreased p-p70S6K levels in IFN-γ-stimulated human keratinocytes, suppressing the IFN-γ induced increase in levels of C-C chemokine ligand 2 mRNA. Interestingly, the increased p70S6K phosphorylation in skin lesions of AD model mice was attenuated by RGE treatment. In conclusion, RGE is a potential therapy against inflammatory responses involving the p70S6K signaling pathway.

【 授权许可】

Unknown