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Inhibitory effects of [6]‐gingerol on PMA‐induced COX‐2 expression and activation of NF‐κB and p38 MAPK in mouse skin
Author(s) -
Kim Sue Ok,
Chun KyungSoo,
Kundu Joydeb Kumar,
Surh YoungJoon
Publication year - 2004
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.552210107
Subject(s) - zingiberaceae , p38 mitogen activated protein kinases , mapk/erk pathway , nf κb , gingerol , protein kinase a , transcription factor , prostaglandin e2 , chemistry , kinase , tumor promotion , phorbol , pharmacology , prostaglandin , protein kinase c , signal transduction , biochemistry , biology , endocrinology , gene , carcinogenesis , ecology , rhizome , chromatography
[6]‐Gingerol, a major pungent ingredient of ginger (Zingiber officinale Roscoe, Zingiberaceae), has a wide array of pharmacologic effects. Previous studies have demonstrated that [6]‐gingerol inhibits mouse skin tumor promotion and anchorage‐independent growth of cultured mouse epidermal cells stimulated with epidermal growth factor. Cyclooxygenase‐2 (COX‐2), a key enzyme in the prostaglandin biosynthesis, has been recognized as a molecular target for many anti‐inflammatory as well as chemopreventive agents. Topical application of [6]‐gingerol inhibited phorbol 12‐myristate 13‐acetate ‐induced COX‐2 expression. One of the essential transcription factors responsible for COX‐2 induction is NF‐κB. [6]‐Gingerol suppressed NF‐κB DNA binding activity in mouse skin. In addition, [6]‐gingerol inhibited the phoshorylation of p38 mitogen‐activated protein kinase which may account for its inactivation of NF‐κB and suppression of COX‐2 expression.