期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 22, 期 20, 页码 -出版社
MDPI
DOI: 10.3390/ijms222011107
关键词
atorvastatin ester; hyperlipidemia; RNA-sequencing; PPAR-signaling pathway; gene expression
资金
- Scientific Research Foundation of the Education Department of Liaoning Province
- Scientific Research Staring Foundation for the Returned Overseas Scholars, Shenyang Pharmaceutical University [GGJJ2021101]
- National Science and Technology Major Project of the Ministry of Science and Technology of China [2018ZX09735005]
- National Natural Science Foundation of China [81973293]
- Foundation Committee of Basic and Applied Basic Research of Guangdong Province [2019A1515110482]
- Shenzhen Natural Science Foundation [JCYJ20190808171803553]
Through research on a rat model induced by high-fat diet, it was found that atorvastatin ester (Ate) can improve metabolic disorder caused by hyperlipidemia, and regulate lipid metabolism by modulating the PPAR signaling pathway and HMGCR gene expression.
Atorvastatin ester (Ate) is a structural trim of atorvastatin that can regulate hyperlipidemia. The purpose of this study was to evaluate the lipid-lowering effect of Ate. Male Sprague Dawley (SD) rats were fed a high-fat diet for seven months and used as a hyperlipidemia model. The lipid level and liver function of the hyperlipidemia rats were studied by the levels of TG, TC, LDL, HDL, ALT, and AST in serum after intragastric administration with different doses of Ate. HE staining was used to observe the pathological changes of the rat liver and gastrocnemius muscle. The lipid deposits in the liver of rats were observed by staining with ORO. The genes in the rat liver were sequenced by RNA-sequencing. The results of the RNA-sequencing were further examined by qRT-PCR and western blotting. Biochemical test results indicated that Ate could obviously improve the metabolic disorder and reduce both the ALT and AST levels in serum of the hyperlipidemia rats. Pathological results showed that Ate could improve HFD-induced lipid deposition and had no muscle toxicity. The RNA-sequencing results suggested that Ate affected liver lipid metabolism and cholesterol, metabolism in the hyperlipidemia-model rats may vary via the PPAR-signaling pathway. The western blotting and qRT-PCR results demonstrated the Ate-regulated lipid metabolism in the hyperlipidemia model through the PPAR-signaling pathway and HMGCR expression. In brief, Ate can significantly regulate the blood lipid level of the model rats, which may be achieved by regulating the PPAR-signaling pathway and HMGCR gene expression.
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