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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 PLoS+One
2018 ; 13
(7
): e0200508
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English Wikipedia
Arecoline inhibits the growth of 3T3-L1 preadipocytes via AMP-activated protein
kinase and reactive oxygen species pathways
#MMPMID30011295
Tian ZH
; Weng JT
; Shih LJ
; Siao AC
; Chan TY
; Tsuei YW
; Kuo YC
; Wang TS
; Kao YH
PLoS One
2018[]; 13
(7
): e0200508
PMID30011295
show ga
The present study was designed to investigate the pathways involved in the effect
of betel nut arecoline on cell viability in 3T3-L1 preadipocytes. Arecoline, but
not arecaidine or guvacine, inhibited preadipocyte viability in a concentration-
and time-dependent manner. Arecoline arrested preadipocyte growth in the G2/M
phase of the cell cycle; decreased the total levels of cyclin-dependent kinase 1
(CDK1), p21, and p27 proteins; increased p53 and cyclin B1 protein levels; and
had no effect on CDK2 protein levels. These results suggested that arecoline
selectively affected a particular CDK subfamily. Arecoline inhibited
AMP-activated protein kinase (AMPK) activity; conversely, the AMPK activator,
AICAR, blocked the arecoline-induced inhibition of cell viability. Pre-treatment
with the antioxidant, N-acetylcysteine, prevented the actions of arecoline on
cell viability, G2/M growth arrest, reactive oxygen species (ROS) production, and
the levels of CDK1, p21, p27, p53, cyclin B1, and phospho-AMPK proteins. These
AMPK- and ROS-dependent effects of arecoline on preadipocyte growth may be
related to the mechanism underlying the modulatory effect of arecoline on body
weight.