GANODERMA LUCIDUM SPORE LIPID INDUCES PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR ALPHA ACTIVITY
Article first published online: 3 OCT 2011
© 2011 Wiley Periodicals, Inc.
Journal of Food Biochemistry
Volume 35, Issue 5, pages 1508–1513, October 2011
How to Cite
HUANG, Z., FANG, F. and WONG, C.-W. (2011), GANODERMA LUCIDUM SPORE LIPID INDUCES PEROXISOME PROLIFERATOR-ACTIVATED RECEPTOR ALPHA ACTIVITY. Journal of Food Biochemistry, 35: 1508–1513. doi: 10.1111/j.1745-4514.2010.00472.x
- Issue published online: 3 OCT 2011
- Article first published online: 3 OCT 2011
- Accepted for Publication January 28, 2010
FIG. S1. EFFECTS OF GS AND FATTY ACIDS ON CELL VIABILITY
HepG2 cells were incubated with 50 µM of different fatty acids for 24 h. Cell viability was measured by the CellTiter-Glo assay kit (Promega). 1 × GS = 0.001% GS in culturing medium. DMSO control was set at 100%. Results represent mean ± SD.
FIG. S2. EFFECTS OF FATTY ACIDS ON PPARα ACTIVITY
HepG2 cells were transfected with pCDNA4v5-HisB-PPARα full length expression plasmid and pGL3-PPAR-response elements-luciferase reporter plasmid. Cells were then treated with 50 µM oleic acid, stearic acid, palmitic acid or palmitoleic acid for 24 h. Relative expression is presented as the fold of expression level of DMSO treatment. **P < 0.01.
FIG. S3. FATTY ACIDS AND GS DID NOT AFFECT PPARα MRNA EXPRESSION IN HEPG2
HepG2 cells were incubated with 100 × GS, 50 µM oleic acid, stearic acid, palmitic acid or palmitoleic acid for 24 h. Relative expression level of PPARα was normalized with β-actin and presented as the fold of DMSO treatment. 100 × GS = 0.1% GS in culturing medium. Values are shown as mean ± SEM of three independent experiments.
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