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Mol Cell Biochem. 2017 Jan;424(1-2):163-172. doi: 10.1007/s11010-016-2851-6. Epub 2016 Oct 24.

Dietary flavones counteract phorbol 12-myristate 13-acetate-induced SREBP-2 processing in hepatic cells.

Author information

1
Food and Nutritional Sciences Programme, School of Life Sciences, Faculty of Science, The Chinese University of Hong Kong, Shatin, Hong Kong.
2
Department of Food Science, National Chiayi University, Chiayi City, Taiwan, ROC.
3
Food and Nutritional Sciences Programme, School of Life Sciences, Faculty of Science, The Chinese University of Hong Kong, Shatin, Hong Kong. laikleung@cuhk.edu.hk.
4
Biochemistry Programmes, School of Life Sciences, Faculty of Science, The Chinese University of Hong Kong, Shatin, Hong Kong. laikleung@cuhk.edu.hk.
5
Food and Nutritional Sciences/Biochemistry Programme, School of Life Sciences, The Chinese University of Hong Kong, Rm.507C MMW Bldg, Shatin, N.T., Hong Kong. laikleung@cuhk.edu.hk.

Abstract

Consumption of fruits and vegetables is generally regarded as beneficial to plasma lipid profile. The mechanism by which the plant foods induce desirable lipid changes remains unclear. SREBP-2 is crucial in cholesterol metabolism, and it is a major regulator of the cholesterol biosynthesis enzyme HMGCR. Our lab has previously illustrated that apigenin and luteolin could attenuate the nuclear translocation of SREBP-2 through an AMPK-dependent pathway. In the present study, these two flavones were studied for their ability to deter the same in an AMPK-independent signaling route. The processing of SREBP-2 protein was promoted by phorbol 12-myristate 13-acetate (PMA) in the hepatic cells WRL and HepG2, and the increased processing was reversed by apigenin or luteolin co-administration. EMSA results demonstrated that the PMA-induced DNA-binding activity was weakened by the flavones. The increased amount of nuclear SREBP-2 in cells was attenuated by the flavonoid as shown by immunocytochemical imaging. Quantitative reverse transcriptase-polymerase chain reaction assay demonstrated that the transcription of HMGCR under both flavone treatments was reduced. However, apigenin appeared to be stronger than luteolin in restraining PMA-induced HMGCR mRNA expression. Since PMA is a diacylglycerol analog, these findings might have some physiological implications.

KEYWORDS:

Apigenin; HMGCR; Luteolin; Nuclear translocation; PKC-dependent pathway; SREBP-2

PMID:
27778136
DOI:
10.1007/s11010-016-2851-6
[Indexed for MEDLINE]

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