Sanghuangporus vaninii extract ameliorates hyperlipidemia in rats by mechanisms identified with transcriptome analysis

Author:

Gao Ning12ORCID,Liu Yuanzhen12,Liu Guangjie12,Liu Bo3ORCID,Cheng Yupeng12

Affiliation:

1. Key Laboratory of Basic and Application Research of Beiyao (Heilongjiang University of Chinese Medicine), Ministry of Education Harbin China

2. School of Pharmacy Heilongjiang University of Chinese Medicine Harbin China

3. School of Pharmaceutical Engineering Heilongjiang Agricultural Reclamation Vocational College Harbin China

Abstract

AbstractThe increasing incidence of hyperlipidemia is a serious threat to public health. The development of effective and safe lipid‐lowering drugs with few side effects is necessary. The purpose of this study was to assess the lipid‐lowering activity of Sanghuangporus vaninii extract (SVE) in rat experiments and reveal the molecular mechanism by transcriptome analysis. Hyperlipidemia was induced in the animals using a high‐fat diet for 4 weeks. At the end of the 4th week, hyperlipidemic rats were assigned into two control groups (model and positive simvastatin control) and three treatment groups that received SVE at 200, 400, or 800 mg kg−1 day−1 for another 4 weeks. A last control group comprised normal chow‐fed rats. At the end of the 8th week, rats were sacrificed and lipid serum levels, histopathology, and liver transcriptome profiles were determined. SVE was demonstrated to relieve the lipid disorder and improve histopathological liver changes in a dose‐dependent manner. The transcriptomic analysis identified changes in hepatocyte gene activity for major pathways including steroid biosynthesis, bile secretion, cholesterol metabolism, AMPK signaling, thyroid hormone signaling, and glucagon signaling. The changed expression of crucial genes in the different groups was confirmed by qPCR. Collectively, this study revealed that SVE could relieve hyperlipidemia in rats, the molecular mechanism might be to promote the metabolism of lipids and the excretion of cholesterol, inhibit the biosynthesis of cholesterol by activating the AMPK signaling pathway, the thyroid hormone signaling pathway, and the glucagon signaling pathway.

Funder

National Natural Science Foundation of China

Publisher

Wiley

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