The effect of Monascus secondary metabolites, monascin and ankaflavin, on adipogenesis and lipolysis activity in 3T3-L1 cells

• Main Authors: Pey-Chyi Jou, 周珮祺
• Other Authors: Tzu-Ming Pan
• Format: Others
• Language: zh-TW
• Published: 2010
• Online Access: http://ndltd.ncl.edu.tw/handle/66747305243670103324

碩士 === 國立臺灣大學 === 微生物與生化學研究所 === 98 === The aim of the present work is to investigate the effects of Monascus secondary metabolites, monascin (MS) and ankaflavin (AK), on cell proliferation, adipogenesis, lipolysis and heparin-releasable lipoprotein lipase (HR-LPL) in 3T3-L1 preadipocyte. MS and AK inhibit the proliferation of 3T3-L1 cells in a dose-dependent fashion. At the 8 μg/mL concentration MS inhibits proliferation for 80.5% after 48 hr, where as AK for 69.2%. Adipogenesis is inhibited by MS and AK without dose-dependency. TG is decreased 37.1% and 41.1% by treating 0.125 μg/mL MS and AK. Adipocyte-specific transcription factors peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer binding protein β (C/EBPβ), C/EBPδ and C/EBPα mRNA levels are measured by real-time polymerase chain reaction and protein levels by Western blot. The expression of the four transcriptional factors analysed (PPARγ, C/EBPβ, C/EBPδ and C/EBPα) is reduced at the initial and the middle period. At the later period, there is no effect on the expression of PPARγ and C/EBPα by treating MS and AK. The adipocyte-specific transcription factors PPARγ, C/EBPβ and C/EBPα are downregulated after the treatment with 2 μg/mL MS (43.3%, 33.7%, and 48.5% reduction) and 2 μg/mL AK (76.1%、43.5%、63.3%) in translational level by Westen blot. Furthermore, both MS and AK increase basal lipolysis of mature adipocytes by 113.2% and 278.3% up-regulation. And both MS and AK reduce the activity of heparin-releasable lipoprotein lipase by 45.3% and 58.1% reduction. This study reveals for the first time that Monascus secondary metabolites, MS and AK, can prevent the differentiatioin of preadipocyte and stimulate basal lipolysisi of mature adipocytes, avoiding the accumulation of lipid.