The Schisandra-Salvia-Hawthorn herbal formulation demonstrates therapeutic efficacy in ameliorating hyperlipidemia
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Updated: Nov 1, 2026
Network Pharmacology Prediction and Metabolomics Validation of the Mechanism of Fructus Phyllanthi against Hyperlipidemia
Published on: April 7, 2023
Nannan Xing1, Huaidong Qu2,3, Ying Jiang1
1College of Basic Medicine, Heilongjiang University of Chinese Medicine, Harbin, China.
Introduction:
This study investigates the potential efficacy and action mechanism of a herbal formulation comprising Schisandra chinensis, Salvia miltiorrhiza and Hawthorn (SSH) in the treatment of hyperlipidemia.
Methods:
A hyperlipidemic cell model was established by free fatty acid (FFA)-induced HepG2 cells and a hyperlipidemic mouse model was established by high-fat diet (HFD)-induced C57BL/6 mice. Cell viability of HepG2 cells was assessed by MTT assay. Serum lipid profiles (TC, TG, LDL-C, HDL-C) were quantified via the corresponding kits. Hepatic tissue pathology was evaluated via Oil Red O staining and HE staining. Serum inflammatory cytokines (TNF-α and IL-6) were measured through ELISA. The mRNA and protein expression of seven key targets (APOB, LDLR, OLR1, PPARG, PRKCA, RXRA, NCF1) identified via network pharmacology prediction, were detected using qRT-PCR and Western blot. Besides, protein levels of p-p65 and p65 were detected by Western blot. Immunofluorescence staining was used to monitor p65 subcellular distribution, and DCFH-DA-based fluorescence detection was conducted to assess ROS production.
Results:
In FFA-induced HepG2 cells, TC, TG, and lipid accumulation were reduced after SSH treatment. In HFD-induced mice, SSH treatment attenuated HFD-induced increases in serum TC, TG, and LDL-C levels, while elevating the level of HDL-C. It also reduced hepatic lipid accumulation, hepatic injury and expression of TNF-α and IL-6. Mechanistically, SSH formulation reversed HFD-driven dysregulation of the predicted targets: it downregulated the expression of APOB, OLR1, PRKCA, RXRA, PPARG and NCF1, and upregulated the expression of LDLR. FFA caused increases of OLR1 protein expression, PRKCA protein expression and phosphorylation of NF-κB p65 as well as ROS production in HepG2 cells, which were reversed by SSH treatment.
Conclusion:
The SSH formulation mitigated hyperlipidemia by restoring lipid homeostasis and suppressing inflammation. Its efficacy was mediated through a multi-target mechanism, coordinately regulating lipoprotein metabolism (APOB/LDLR), oxidative stress and inflammatory signaling (OLR1/PRKCA/NCF1), and nuclear receptor activity (PPARG/RXRA).
