ArticleBMC complementary medicine and therapies2022
Exploring the protective mechanism of baicalin in treatment of atherosclerosis using endothelial cells deregulation model and network pharmacology.
Article in BMC complementary medicine and therapies, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.
- Preclinical Evaluation of Baicalin for the Treatment of Diabetic Nephropathy: A Systematic Review and Meta-Analysis.Planta medica · 2025Pooled it
- NR1D1-Mediated Suppression of JAK1/STAT3 Signaling Contributes to the Therapeutic Effects of Triptolide in Rheumatoid Arthritis.Mediators of inflammation · 2026Article
- Baicalin: bridging traditional medicine and modern science in food and functional applications.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Multi-target mechanisms and therapeutic potential of Dahuang Zhechong pill in lower extremity peripheral artery disease: a structured narrative review.Frontiers in pharmacology · 2026Review
- Pharmacological mechanisms by which baicalin ameliorates cardiovascular disease.Frontiers in pharmacology · 2024Review
- Phytochemical analysis,Frontiers in pharmacology · 2024Article
- Molecular targets and therapeutic potential of baicalein: a review.Drug target insightsReview
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBaicalin is a generally available flavonoid with potent biological activity. The present study aimed to assess the underlying mechanism of baicalin in treatment of atherosclerosis (AS) with the help of network pharmacology, molecular docking and experimental validation.
methodsThe target genes of baicalin and AS were identified from public databases, and the overlapping results were considered to be baicalin-AS targets. Core target genes of baicalin were obtained through the PPI network and validated by a clinical microarray dataset (GSE132651). Human aortic endothelial cells (HAECs) were treated with Lipopolysaccharide (LPS) to construct an endothelial injury model. The expression of NOX4 was examined by real-time qPCR and western blot. Flow cytometry was used to detect intracellular levels of reactive oxygen species (ROS). Furthermore, HAECs were transfected with NOX4-specific siRNA and then co-stimulated with baicalin and LPS to investigate whether NOX4 was involved in the anti-oxidative stress effects of baicalin.
resultsIn this study, baicalin had 45 biological targets against AS. Functional enrichment analysis demonstrated that most targets were involved in oxidative stress. Using the CytoHubba plug-in, we obtained the top 10 genes in the PPI network ranked by the EPC algorithm. Molecular docking and microarray dataset validation indicated that NOX4 may be an essential target of baicalin, and its expression was significantly suppressed in AS samples compared to controls. In endothelial injury model, intervention of HAECs with baicalin increased the expression levels of NOX4 and NOS3 (eNOS), and decreased LPS-induced ROS generation. After inhibition of NOX4, the anti-ROS-generating effect of baicalin was abolished.
conclusionCollectively, we combined network pharmacology and endothelial injury models to investigate the anti-AS mechanism of baicalin. The results demonstrate that baicalin may exert anti-oxidative stress effects by targeting NOX4, providing new mechanisms and insights to baicalin for the treatment of AS.
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