Validation experiment designed to validate causal mechanisms targeting ACSL1, SCD1, PPARγ in C57BL/6J mice. Primary outcome: serum lipid levels (TC, TG, HDL-C, LDL-C) and body weight reduction
This comprehensive animal study investigated the lipid-lowering effects and mechanisms of myricanol using a high-fat diet (HFD)-induced hyperlipidemic mouse model. C57BL/6J mice were fed an olive oil and lard mixture for 8 weeks to establish hyperlipidemia, then randomly divided into control, rosiglitazone positive control (0.78 mg/kg), low-dose myricanol (100 mg/kg), and high-dose myricanol (150 mg/kg) groups. Treatment continued for 25 days. The study employed multiple analytical approaches including serum lipid measurements, histopathological examination, Western blotting for protein expression analysis, metabolomics, 16S rRNA sequencing for gut microbiota analysis, RNA sequencing, ELISA, immunofluorescence staining, double-fluorescence labeling, and cellular thermal shift assay (CETSA) to comprehensively evaluate mechanisms. The research revealed that myricanol significantly reduced body weight within 7 days, normalized serum lipid levels (TC, TG, HDL-C, LDL-C), reduced hepatic lipid droplet accumulation, and decreased epididymal fat volume through modulation of the PPARγ/ACSL1/SCD1 signaling pathway.
8-week HFD induction followed by 25-day treatment with myricanol (100 or 150 mg/kg) or rosiglitazone (0.78 mg/kg). Multi-omics analysis including Western blotting, metabolomics, 16S rRNA sequencing, RNA sequencing, ELISA, immunofluorescence, and CETSA
Reduction in serum lipid levels, decreased hepatic lipid accumulation, weight loss, and modulation of lipid metabolism pathways
Significant improvement in serum lipid profile, histopathological improvements in liver and adipose tissue, upregulation of beneficial metabolic genes
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