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Evodiamine inhibits adipogenesis via the EGFR–PKCα–ERK signaling pathway
Author(s) -
Wang Ting,
Wang Youxue,
Yamashita Hitoshi
Publication year - 2009
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2009.10.046
Subject(s) - adipogenesis , mapk/erk pathway , chemistry , evodiamine , signal transduction , microbiology and biotechnology , protein kinase c , pharmacology , endocrinology , medicine , biology , biochemistry , adipose tissue
The molecular mechanism of the anti‐adipogenic effect of evodiamine (which has several capsaicin‐like pharmacological actions) was investigated. The evodiamine effect was not blocked by the specific TRPV1 antagonist capsazepine in 3T3‐L1 preadipocytes, whereas its effect was greatly curtailed by inhibitors of protein kinase C (PKC) and epidermal growth factor receptor (EGFR). Signal analyses showed that evodiamine stimulated the phosphorylation of EGFR, PKCα, and ERK, all of which were reduced by an EGFR inhibitor. Silencing experiments of EGFR mRNA supported the involvement of these signaling molecules in the inhibitory effect of evodiamine. An unidentified mechanism whereby evodiamine inhibits adipogenesis via the EGFR–PKCα–ERK signaling pathway was revealed.