AI Article Synopsis
- Whole-transcriptome analysis and western blotting showed that sauchinone affects cholesterol metabolism in HepG2 cells by downregulating PCSK9 and upregulating LDLR, leading to increased LDL-cholesterol uptake.
- Oral administration of sauchinone in obese mice confirmed this effect, resulting in lower serum LDL-C levels and improved hepatic LDLR through PCSK9 inhibition.
- The findings suggest that sauchinone may help reduce liver fat (hepatic steatosis) by influencing the expression of genes associated with cholesterol regulation via SREBP-2.
Article Abstract
Whole-transcriptome analysis and western blotting of sauchinone-treated HepG2 cells demonstrated that sauchinone regulated genes relevant to cholesterol metabolism and synthesis. In particular, it was found that the expression of proprotein convertase subtilisin/kexin type 9 (PCSK9) was downregulated, and the expression of low density lipoprotein receptor (LDLR) was upregulated in sauchinone-treated HepG2 cells. Consequently, LDL-cholesterol (LDL-C) uptake was increased. As a transcriptional regulator of PCSK9 expression, sterol regulatory elements binding protein-2 (SREBP-2) was proposed by transcriptome analysis and western blotting. Oral administration of sauchinone increased hepatic LDLR through PCSK9 inhibition in obese mice and showed the reduced serum LDL-C levels and downstream targets of SREBP-2. Thus, it is evident that sauchinone reduces hepatic steatosis by downregulating the expression of hepatic PCSK9 via SREBP-2.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5928089 | PMC |
| http://dx.doi.org/10.1038/s41598-018-24935-6 | DOI Listing |
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