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10.1371/journal.pone.0200508

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suck abstract from ncbi


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      PLoS+One 2018 ; 13 (7 ): e0200508
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  • 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.
  • |3T3-L1 Cells [MESH]
  • |AMP-Activated Protein Kinases/*metabolism [MESH]
  • |Adipocytes/cytology/*metabolism [MESH]
  • |Animals [MESH]
  • |Arecoline/*pharmacology [MESH]
  • |Cell Cycle Proteins/biosynthesis [MESH]
  • |G2 Phase Cell Cycle Checkpoints/*drug effects [MESH]
  • |Gene Expression Regulation/drug effects [MESH]
  • |Mice [MESH]


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