Enhanced Effects of Xanthohumol Plus Honokiol on Apoptosis in 3T3-L1 Adipocytes
Article first published online: 6 SEP 2012
2008 North American Association for the Study of Obesity (NAASO)
Volume 16, Issue 6, pages 1232–1238, June 2008
How to Cite
Yang, J.-Y., Della-Fera, M. A., Rayalam, S. and Baile, C. A. (2008), Enhanced Effects of Xanthohumol Plus Honokiol on Apoptosis in 3T3-L1 Adipocytes. Obesity, 16: 1232–1238. doi: 10.1038/oby.2008.66
- Issue published online: 6 SEP 2012
- Article first published online: 6 SEP 2012
- Received September 21, 2007; Accepted December 08, 2007
Objective: To study the effects of xanthohumol (XN), a flavonoid found in hops (Humulus lupulus) and honokiol (HK), a lignan isolated from Magnolia officinalis, alone and in combination, on apoptotic signaling in 3T3-L1 adipocytes.
Methods and Procedures: 3T3-L1 mature adipocytes were incubated with various concentrations of XN and HK alone and in combination. Viability and apoptosis were quantified using an MTS-based cell viability assay and single-stranded DNA assay, respectively. Expression of apoptosis related proteins including cleaved poly(ADP-ribose) polymerase (PARP), cytochrome c, Bcl-2, caspase-3/7, phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and Akt was analyzed by western blotting.
Results: Combinations of XN and HK significantly decreased viability and induced apoptosis in a dose-dependent manner and more than the additive responses to XN and HK alone. Western blot analysis showed an increase in cleaved PARP and cytochrome c release and decrease in expression of Bcl-2 protein by XN plus HK, whereas XN and HK individually had no effect. Furthermore, the combination of XN and HK activated PTEN and inactivated Akt by decreasing levels of phosphorylated PTEN and phosphorylated Akt.
Discussion: We demonstrated that although XN and HK showed little or no effect as individual compounds, in combination (XN plus HK) they showed enhanced activity in inducing apoptosis via the cytochrome c/caspase-3/PARP and PTEN/Akt pathways in 3T3-L1 adipocytes.