| In vitro: |
| Food Chem Toxicol. 2011 Jan;49(1):166-72. | | 7,8-didehydrocimigenol from Cimicifugae rhizoma inhibits TNF-α-induced VCAM-1 but not ICAM-1expression through upregulation of PPAR-γ in human endothelial cells.[Pubmed: 20946932] | Activators of PPAR have been demonstrated to inhibit the induction of VCAM-1 but not ICAM-1 in human endothelial cells (EC). During the screening of anti-inflammatory activity of traditional herbs, we found 7,8-Didehydrocimigenol (7,8-DHC), one of active triterpenoids of Cimicifugae rhizoma (C. rhizoma) increases PPAR-γ expression in EC in a time- and dose-dependent manner.
METHODS AND RESULTS:
Therefore, we asked whether 7,8-Didehydrocimigenol selectively inhibits the expression of VCAM-1 but not ICAM-1 in TNF-α-activated EC via upregulation of PPAR-γ. Treatment with 7,8-Didehydrocimigenol or PPAR-γ agonists (GW1929, troglitazone) inhibited the expression of VCAM-1 but not ICAM-1. 7,8-Didehydrocimigenol significantly inhibited NF-kB activity via inhibition of phosphorylation of IkB and it also inhibited phosphorylation of ERK1/2 and Akt but not PKC. Finally, attachment of monocytes (U937) to EC by TNF-α was significantly reduced by 7,8-Didehydrocimigenol .
CONCLUSIONS:
These results indicate that upregualtion of PPAR-γ by 7,8-Didehydrocimigenol in EC inhibits NF-kB activity of TNF-α-activated EC which leads to selective inhibition of VCAM-1 expression. In addition, ERK1/2 and Akt signal pathways are involved in differential regulation by 7,8-Didehydrocimigenol. We concluded that 7,8-Didehydrocimigenol can be used for the treatment of cardiovascular disorders such as atherosclerosis. |
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