4.7 Article

Diaporisoindole B Reduces Lipid Accumulation in THP-1 Macrophage Cells via MAPKs and PPAR?-LXR? Pathways and Promotes the Reverse Cholesterol Transport by Upregulating SR-B1 and LDLR in HepG2 Cells

Journal

JOURNAL OF NATURAL PRODUCTS
Volume 85, Issue 12, Pages 2769-2778

Publisher

AMER CHEMICAL SOC
DOI: 10.1021/acs.jnatprod.2c00715

Keywords

-

Funding

  1. National Natural Science Foundation of China [41906033]
  2. Natural Science Foundation of Guangdong Province of China [2019A1515012084]
  3. Discipline construction project of Guangdong Medical University [4SG22024G]

Ask authors/readers for more resources

In this study, DPB was found to reduce lipid accumulation in THP-1 macrophage-derived foam cells by regulating lipid intake and efflux through modulating gene expression. Additionally, DPB promoted LDL transport in HepG2 cells and inhibited cholesterol and fatty acid synthesis.
Diaporisoindole B (DPB), an isoprenylisoindole alkaloid isolated from the mangrove endophytic fungus Diaporthe sp. SYSU-HQ3, has been proved to have a good anti-inflammatory activity in macrophage cells. In this study, we found that DPB was able to reduce lipid accumulation in THP-1 macrophage-derived foam cells. DPB could inhibit the lipid influx-related gene CD36 and increase the expression of lipid efflux-related genes ATP binding cassette transporter A1 (ABCA1), ATP binding cassette transporter G1 (ABCG1), and scavenger receptor B1 (SR-B1). Moreover, DPB elevated low density lipoprotein receptor (LDLR) protein expression in HepG2 cells, which can increase the transport of LDL. Meanwhile, DPB could downregulate the expression levels of proteins related to cholesterol and fatty acid synthesis. Further study showed that DPB could activate peroxisome proliferator-activated receptor gamma (PPAR??) and inhibit mitogen-activated protein kinase (MAPK) phosphorylation. Taken together, our findings demonstrated that DPB could reduce lipid accumulation in THP-1 macrophage cells by reducing the intake of lipids and promoting the efflux of lipids and also could promote the reverse cholesterol transport (RCT) mechanism by upregulating SR-B1 and LDLR in HepG2 cells.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.7
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available