ArticleCurrent pharmaceutical design2024
Hua-Feng-Dan Alleviates LPS-induced Neuroinflammation by Inhibiting the TLR4/Myd88/NF-κB Pathway: Integrating Network Pharmacology and Experimental Validation.
Article in Current pharmaceutical design, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Regulatory Effects of the PDE8B Inhibitor PF-04957325 on Cognitive Impairment and Neuroinflammation in Aβ-Induced Alzheimer's Disease Mouse Models.Neurochemical research · 2026Article
- Network Pharmacology Analysis and Experimental Validation of Tectoridin in the Treatment of Ischemic Stroke by Inhibiting Apoptosis and Regulating Inflammation.International journal of molecular sciences · 2025Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeuroinflammation is the pathological basis of many neurological diseases, including neurodegenerative diseases and stroke. Hua-Feng-Dan (HFD) is a well-established traditional Chinese medicine that has been used for centuries to treat stroke and various other brain-related ailments.
objectiveOur study aims to elucidate the molecular mechanism by which HFD mitigates neuroinflammation by combining network pharmacology and
methodsTCMSP and SymMap databases were used to extract active compounds and their related targets. The neuroinflammation-related targets were obtained from the GeneCards database. The common targets of HFD and neuroinflammation were used to construct a protein-protein interaction (PPI) network. MCODE plug-in was used to find the hub module genes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were used to dissect the hub module genes. The lipopolysaccharide (LPS)-induced BV2 microglial neuroinflammation model was utilized to assess the therapeutic effects of HFD on neuroinflammation. Western blotting analysis was performed to examine the core target proteins in the TLR4/My- D88/NF-κB signaling pathway, potentially implicated in HFD's therapeutic effects on neuroinflammation. Hoechst 33342 staining and JC-1 staining were employed to evaluate neuronal apoptosis.
resultsThrough network pharmacology, 73 active compounds were identified, with quercetin, beta-sitosterol, luteolin, and (-)-Epigallocatechin-3-Gallate recognized as important compounds. Meanwhile, 115 common targets of HFD and neuroinflammation were identified, and 61 targets were selected as the hub targets utilizing the MCODE algorithm. The results of
conclusionThe findings demonstrated that HFD had an inhibitory effect on LPS-induced neuroinflammation in microglia and elucidated its underlying mechanism. These findings will offer a theoretical foundation for the clinical utilization of HFD in treating neurodegenerative diseases associated with neuroinflammation.
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