ArticleFrontiers in pharmacology2025
Berberine alleviates atherosclerosis by modulating autophagy and inflammation through the RAGE-NF-κB pathway.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Berberine-associated lipid-inflammatory regulation in atherosclerosis: an integrative transcriptomic, single-cell, and in vivo study.Functional & integrative genomics · 2026Article
- Metabolic and Anti-Inflammatory Effects of Berberine-Rationale for Its Therapeutic Potential in Polycystic Ovary Syndrome.International journal of molecular sciences · 2026Review
- A bibliometric analysis of autophagy research in atherosclerosis over the past decade.Medicine · 2026Review
- Microbiota-mediated mechanisms of natural products in atherosclerosis: focus on metabolic and inflammatory pathways.Frontiers in endocrinology · 2026Review
- Dysregulated Redox Signaling and Its Impact on Inflammatory Pathways, Mitochondrial Dysfunction, Autophagy and Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Plant-derived natural products targeting inflammation in treatment of atherosclerosis.Frontiers in pharmacology · 2025Review
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Authors and funding
8 authors.
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Abstract
Introduction: Lipid accumulation and foam cell formation are significant features that expedite the progression of atherosclerosis (AS). Abnormal autophagy is a key factor in the development of AS. The importance of berberine (BBR) in AS has been well established. However, its exact role in regulating autophagy and alleviating atherosclerotic inflammation remains unclear. Purpose: This study was aimed at exploring the role and mechanism of BBR in alleviating AS by activating autophagy and alleviating inflammation. Study design: Network pharmacology predicts the potential mechanism of BBR in regulating AS and verifies this mechanism through Methods: The potential mechanism through which BBR regulates AS was predicted by network pharmacology. Total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein (HDL-C) were measured by administering BBR (100 mg/kg) via the stomach. Hematoxylin and eosin (HE) and oil red O staining were used for histological analysis. Expression levels of the RAGE and p-NF-κB pathways and autophagy-associated proteins were evaluated by immunofluorescence. The ApoE Results: Functional and pathway enrichment analysis demonstrated that BBR significantly modulated the inflammation-related signaling pathways of AS. Additionally, Conclusion: In summary, BBR alleviated the disease progression of AS by regulating the expression of RAGE and p-NF-κB and activating autophagy.
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