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Fermented black ginseng extract prevents UVB-induced inflammation by regulating the nc886-PKR pathway in human keratinocytes.
Kim, Yuna; Sim, Junbo; Jeon, Kyungeun; Ryu, Dehun; Ji, Youngeun; Kim, Youngseok; Kim, Junoh; Jeon, Suwon; Park, Deokhoon; Jung, Eunsun.
Affiliation
  • Kim Y; Biospectrum Life Science Institute, Yongin-si, Gyeonggi-do, Republic of Korea.
  • Sim J; Biospectrum Life Science Institute, Yongin-si, Gyeonggi-do, Republic of Korea.
  • Jeon K; Biospectrum Life Science Institute, Yongin-si, Gyeonggi-do, Republic of Korea.
  • Ryu D; Biospectrum Life Science Institute, Yongin-si, Gyeonggi-do, Republic of Korea.
  • Ji Y; Shinsegae International Inc., Seoul, Republic of Korea.
  • Kim Y; Shinsegae International Inc., Seoul, Republic of Korea.
  • Kim J; Shinsegae International Inc., Seoul, Republic of Korea.
  • Jeon S; Biospectrum Life Science Institute, Yongin-si, Gyeonggi-do, Republic of Korea.
  • Park D; Biospectrum Life Science Institute, Yongin-si, Gyeonggi-do, Republic of Korea.
  • Jung E; Biospectrum Life Science Institute, Yongin-si, Gyeonggi-do, Republic of Korea.
Article de En | MEDLINE | ID: mdl-37961814
ABSTRACT

BACKGROUND:

Continuous exposure of the skin to ultraviolet B (UVB) rays can cause inflammation and photodamage. In previous studies, we observed that the upregulation of nc886, a noncoding RNA (ncRNA), can alleviate UVB-induced inflammation through suppression of the protein kinase RNA (PKR) pathway. We aim to investigate the effect of fermented black ginseng extract (FBGE), which has been shown to increase the expression of nc886, on UVB-induced inflammation in keratinocytes.

METHODS:

To confirm the cytotoxicity of FBGE, MTT assay was performed, and no significant cytotoxicity was found on human keratinocytes. The efficacies of FBGE were assessed through qPCR, Western blotting, and ELISA analysis which confirmed regulation of UVB-induced inflammation.

RESULTS:

The analysis results showed that FBGE inhibited the decrease in nc886 expression and the increase in the methylated nc886 caused by UVB. It also prevented the UVB-induced increase of metalloproteinase-9 (MMP-9), metalloproteinase-1 (MMP-1), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α). Additionally, FBGE suppressed the PKR-MAPK pathways activated by UVB.

CONCLUSION:

These results implicate that FBGE can alleviate UVB-induced inflammation through regulation of the nc886-PKR pathway.
Sujet(s)
Mots clés

Texte intégral: 1 Collection: 01-internacional Base de données: MEDLINE Sujet principal: Kératinocytes / Panax Limites: Humans Langue: En Journal: Photodermatol Photoimmunol Photomed Sujet du journal: ALERGIA E IMUNOLOGIA / DERMATOLOGIA Année: 2024 Type de document: Article

Texte intégral: 1 Collection: 01-internacional Base de données: MEDLINE Sujet principal: Kératinocytes / Panax Limites: Humans Langue: En Journal: Photodermatol Photoimmunol Photomed Sujet du journal: ALERGIA E IMUNOLOGIA / DERMATOLOGIA Année: 2024 Type de document: Article