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Cited by 221

The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.

[6]-Gingerol prevents UVB-induced ROS production and COX-2 expression in vitro and in vivo

Kim, Jin-Kyoung, Kim, Younghwa, Na, Kwang-Min, Surh, Young-Joon, Kim, Tae-Yoon·2007·Free Radical Research

Abstract

[6]-Gingerol, a naturally occurring plant phenol, is one of the major components of fresh ginger (Zingiber officinale Roscoe, Zingiberaceae) and has diverse pharmacologic effects. Here, we describe its novel anti-oxidant, anti-apoptotic, and anti-inflammatory activities in vitro and in vivo. In vitro, pre-treatment with [6]-gingerol reduced UVB-induced intracellular reactive oxygen species levels, activation of caspase-3, -8, -9, and Fas expression. It also reduced UVB-induced expression and transactivation of COX-2. Translocation of NF-kappaB from cytosol to nucleus in HaCaT cells was inhibited by [6]-gingerol via suppression of IkappaBalpha phosphorylation (ser-32). Examination by EMSAs and immunohistochemistry showed that topical application of [6]-gingerol (30 microM) prior to UVB irradiation (5 kJ/m(2)) of hairless mice, also inhibited the induction of COX-2 mRNA and protein, as well as NF-kappaB translocation. These results suggest that [6]-gingerol could be an effective therapeutic agent providing protection against UVB-induced skin disorders.

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Metadata

Authors
Kim, J.-K., Kim, Y., Na, K.-M., Surh, Y.-J., & Kim, T.-Y.
Venue
Free Radical Research
Published
2007-01
Volume
41
Issue
5
Pages
603-614
ISSN
  • 1029-2470 (ISSN-L)
  • 1071-5762
OpenAlex
W2006452078
Cited by
221
References
8
FWCI
7.92
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: [6]-Gingerol prevents UVB-induced ROS production and COX-2 expression in vitro and in vivo. https://app.cochat.ai/papers/10.1080/10715760701209896
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Kim, J.-K., Kim, Y., Na, K.-M., Surh, Y.-J., & Kim, T.-Y. (2007). [6]-Gingerol prevents UVB-induced ROS production and COX-2 expression in vitro and in vivo. Free Radical Research. https://doi.org/10.1080/10715760701209896

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