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Shanhuang Jiangzhi tablets mitigate atherosclerosis by modulating macrophage polarization and inhibiting foam cell
Yingwei Chang1,2, Qing Liu3,4,5, Qixuan Guo5
1Suzhou Medical College of Soochow University, Soochow University, Suzhou 215000, China.
Objectives:
Atherosclerosis significantly contributes to global cardiovascular mortality. Macrophage polarization and foam cell formation via oxidized low-density lipoprotein uptake are key drivers of plaque progression and instability. Targeting these processes may offer a promising therapeutic approach. This study aimed to investigate the potential therapeutic effects of Shanhuang Jiangzhi tablets (SHJZT) using apolipoprotein E-deficient mice and RAW264.7 macrophage-based experimental models.
Methods:
Key assays, including oxidized low-density lipoprotein-induced foam cell formation and lipopolysaccharide (LPS)-induced macrophage polarization, were performed to elucidate the regulatory effects of SHJZT, with a particular focus on the reactive oxygen species (ROS)/Toll-like receptor 4 (TLR4)/NF-κB signaling pathway.
Key Findings:
In vivo, SHJZT treatment significantly attenuated atherosclerotic lesion development, improved lipid metabolism, and enhanced reverse cholesterol transport by regulating ABCA1 and ABCG1 expression, thereby suppressing foam cell formation. Furthermore, SHJZT promoted macrophage polarization from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype. Mechanistic investigations revealed that SHJZT mitigated LPS-induced ROS production and inhibited the activation of the TLR4/NF-κB signaling cascade in vitro. Specifically, SHJZT downregulated key pathway components, including TLR4, MYD88, and phosphorylated NF-κB p65, in high-fat diet-induced atherosclerosis.
Conclusion:
SHJZT exerts anti-atherosclerotic effects by modulating macrophage polarization and inhibiting foam cell formation through the suppression of ROS/TLR4/NF-κB signaling pathway.
Insights
Shanhuang Jiangzhi tablets (SHJZT) reduce atherosclerosis by inhibiting foam cell formation and promoting beneficial macrophage polarization. This involves suppressing the reactive oxygen species (ROS)/Toll-like receptor 4 (TLR4)/NF-κB signaling pathway.
Area of Science:
- Cardiovascular Research
- Immunology
- Pharmacology
Background:
- Atherosclerosis is a leading cause of cardiovascular death.
- Macrophage polarization and foam cell formation are critical in plaque development.
- Targeting these processes offers potential therapeutic strategies.
Purpose of the Study:
- To evaluate the anti-atherosclerotic effects of Shanhuang Jiangzhi tablets (SHJZT).
- To investigate the impact of SHJZT on macrophage polarization and foam cell formation.
- To elucidate the underlying molecular mechanisms involving the ROS/TLR4/NF-κB pathway.
Main Methods:
- Utilized apolipoprotein E-deficient mice and RAW264.7 macrophages.
- Assessed oxidized low-density lipoprotein-induced foam cell formation.
- Analyzed lipopolysaccharide (LPS)-induced macrophage polarization and signaling pathway activation.
Main Results:
- SHJZT treatment reduced atherosclerotic lesions and improved lipid metabolism in vivo.
- SHJZT promoted M2 macrophage polarization and suppressed foam cell formation.
- SHJZT inhibited ROS production and TLR4/NF-κB pathway activation in vitro and in vivo.
Conclusions:
- SHJZT demonstrates significant anti-atherosclerotic properties.
- The therapeutic effects are mediated by modulating macrophage polarization and foam cell formation.
- Suppression of the ROS/TLR4/NF-κB signaling pathway is a key mechanism of action.
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