2. Academic Validation
  3. Methyl protodioscin increases ABCA1 expression and cholesterol efflux while inhibiting gene expressions for synthesis of cholesterol and triglycerides by suppressing SREBP transcription and microRNA 33a/b levels

Methyl protodioscin increases ABCA1 expression and cholesterol efflux while inhibiting gene expressions for synthesis of cholesterol and triglycerides by suppressing SREBP transcription and microRNA 33a/b levels

  • Atherosclerosis. 2015 Apr;239(2):566-70. doi: 10.1016/j.atherosclerosis.2015.02.034.
Weilie Ma 1,  Hang Ding 1,  Xiaohua Gong 1,  Zhen Liu 1,  Yalin Lin 1,  Zhizhen Zhang 2,  Guorong Lin 3
Affiliations

Affiliations

  • 1 Department of Biochemistry and Molecular Biology, Guangdong Medical College, Dongguan, Guangdong, China; Key Laboratory for Medical Molecular Diagnostics of Guangdong Province, Guangdong Medical College, Dongguan, Guangdong, China.
  • 2 Department of Biochemistry and Molecular Biology, Guangdong Medical College, Dongguan, Guangdong, China; Key Laboratory for Medical Molecular Diagnostics of Guangdong Province, Guangdong Medical College, Dongguan, Guangdong, China. Electronic address: zzzhang@gdmc.edu.cn.
  • 3 Department of Biochemistry and Molecular Biology, Guangdong Medical College, Dongguan, Guangdong, China; Key Laboratory for Medical Molecular Diagnostics of Guangdong Province, Guangdong Medical College, Dongguan, Guangdong, China. Electronic address: glin@omegacoffee.com.
PMID: 25733328 DOI: 10.1016/j.atherosclerosis.2015.02.034
Abstract

Sterol regulatory element-binding proteins (SREBPs) regulate homeostasis of LDL, HDL and triglycerides. This study was aimed to determine if inhibition of SREBPs by methyl protodioscin (MPD) regulates downstream gene and protein expressions of lipid metabolisms. In THP-1 macrophages, MPD increases levels of ABCA1 mRNA and protein in dose- and time-dependent manners, and apoA-1-mediated Cholesterol efflux. The underlying mechanisms for the effects is that MPD inhibits the transcription of SREBP1c and SREBP2, and decreases levels of MicroRNA 33a/b hosted in the introns of SREBPs, which leads to reciprocally increase ABCA1 levels. In HepG2 cells, MPD shows the same effects as these observed in THP-1 macrophages. MPD also decreases the gene expressions of HMGCR, FAS and ACC for Cholesterol and fatty acid synthesis. MPD further promotes LDL receptor through reducing the PCSK9 level. Collectively, the study demonstrates that MPD potentially increase HDL Cholesterol while reducing LDL Cholesterol and triglycerides.

Keywords

ABCA1; HDL; LDL; Methyl protodioscin; SREBP; miR-33a/b.

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