ArticleCombinatorial chemistry & high throughput screening2025
Mechanism of HJ11 Decoction in the Treatment of Atherosclerosis Based on Network Pharmacology and Experimental Validation.
Article in Combinatorial chemistry & high throughput screening, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The bidirectional enigma of glaucoma and anxiety: from neuroinflammatory mechanisms to mind-body integrated therapies.Frontiers in psychiatry · 2025Pooled it
- Chinese Medicine Formula HJ11 Alleviates Atherosclerosis by Inactivating the TLR4/MyD88/IκB-α Pathway and Modulating the Heart-Gut Axis Response.Journal of inflammation research · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
backgroundHJ11 (HJ11 decoction), which is based on the traditional prescription Si-Miao-Yong-An decoction, has exerted a remarkable effect on atherosclerosis (AS). Nevertheless, the main components and underlying mechanisms of HJ11 for treating AS remain unclear. AIM OF THE STUDY: This study was designed to elucidate the mechanism of HJ11 in the treatment of AS through network pharmacology and in vivo experimental validation.
methodsNetwork pharmacology was employed to explore the primary bioactive components and targets of HJ11. AS-related genes were obtained from the GeneCards and DisGeNET databases and screened for intersections with HJ11. A herb-compound-target interaction network was constructed by Cytoscape 3.9.1, and molecular docking analyses were constructed on key targets. By using a mouse model, the mechanism of action of HJ11 was further confirmed.
resultsA total of 231 active components of HJ11, 1681 AS-related genes, and 156 common targets were identified. Through the establishment of numerous networks, it was discovered that the main association of the mechanism of HJ11 in AS therapy pertained to anti-inflammation. Important substances included quercetin, kaempferol, and luteolin, while TNF-α, AKT1, IL-6, and VEGFA were the main targets. Molecular docking demonstrated that there were favorable binding interactions between active drugs (quercetin, kaempferol, and luteolin) and targets (TNF-α, AKT1, IL-6, and VEGFA). In the in vivo study, HJ11 reduced the expression of TNF-α, AKT1, IL-6, and VEGFA at both the mRNA and protein levels, inhibited atherosclerotic lesions in AS mouse models, and retarded the development of retroarterioid sclerosis.
conclusionsHJ11 can inhibit inflammation and the progression of AS, and the mechanism might involve downregulating the expression of TNF-α, AKT1, IL-6, and VEGFA.
Indexed as
Identifiers
39844546What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.