The Schisandra-Salvia-Hawthorn herbal formulation demonstrates therapeutic efficacy in ameliorating hyperlipidemia
4 affiliations
- 1College of Basic Medicine, Heilongjiang University of Chinese Medicine
- 2Health Center, Harbin Normal University
- 3College of Pharmacy, Heilongjiang University of Chinese Medicine
- 4Experimental Teaching and Practical Training Center, Heilongjiang University of Chinese Medicine
Abstract
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).
Related
- Gut microbiota as a potential mediator of the disease-ameliorating effects of molecular hydrogen: mechanisms and therapeutic perspectives
- Therapeutic Potential of [(AP)₂M]: A Rationally Designed Polyherbal Formulation for Antidiabetic and Antihyperlipidemic Effects in Alloxan-Induced Diabetic Mice.
- Wide-Targeted Metabolomics Combined with Network Pharmacology Analysis Reveals Metabolite Dynamics and Optimal Harvest Time Across Developmental Stages in Schisandra chinensis (Turcz.) Baill.
- BPC-157 as an Investigational Peptide Therapeutic: Biopharmaceutical Challenges, Formulation Strategies, and Translational Development Barriers
- Atorvastatin improves hyperlipidemia-induced erectile dysfunction via PKA-associated eNOS phosphorylation at the Ser633 site
BibTeX
@article{xing2026schisandrasalviahawthorn,
title = {{The Schisandra-Salvia-Hawthorn herbal formulation demonstrates therapeutic efficacy in ameliorating hyperlipidemia}},
author = {Nannan Xing and Huaidong Qu and Ying Jiang and Pengling Ge and Wei Ma},
journal = {Frontiers in Pharmacology},
year = {2026},
month = oct,
doi = {10.3389/fphar.2026.1893568},
url = {https://www.frontiersin.org/articles/10.3389/fphar.2026.1893568/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - The Schisandra-Salvia-Hawthorn herbal formulation demonstrates therapeutic efficacy in ameliorating hyperlipidemia
AU - Nannan Xing
AU - Huaidong Qu
AU - Ying Jiang
AU - Pengling Ge
AU - Wei Ma
PY - 2026
DA - 2026/10/16
JO - Frontiers in Pharmacology
DO - 10.3389/fphar.2026.1893568
UR - https://www.frontiersin.org/articles/10.3389/fphar.2026.1893568/full
AB - 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).
SN - 1663-9812
ER -