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lüll Evodiamine inhibits adipogenesis via the EGFR-PKCalpha-ERK signaling pathway Wang T; Wang Y; Yamashita HFEBS Lett 2009[Nov]; 583 (22): 3655-9The 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, PKCalpha, 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-PKCalpha-ERK signaling pathway was revealed.|3T3-L1 Cells[MESH]|Adipogenesis/*drug effects[MESH]|Animals[MESH]|Blotting, Western[MESH]|Enzyme Inhibitors/pharmacology[MESH]|ErbB Receptors/antagonists & inhibitors/genetics/*metabolism[MESH]|Extracellular Signal-Regulated MAP Kinases/*metabolism[MESH]|Mice[MESH]|Mice, Knockout[MESH]|Phosphorylation/drug effects[MESH]|Plant Extracts/*pharmacology[MESH]|Protein Kinase C-alpha/antagonists & inhibitors/*metabolism[MESH]|Quinazolines/*pharmacology[MESH]|RNA Interference[MESH]|Reverse Transcriptase Polymerase Chain Reaction[MESH]|Signal Transduction/drug effects[MESH]|TRPV Cation Channels/deficiency/genetics[MESH]|Tyrphostins/pharmacology[MESH] |