ArticleJournal of molecular histology2026
Aconiti Lateralis Radix Praeparata active ingredients of Heishunpian potential on LPS-induced Nrf-2/NQO1/HO-1 and Smad3/Akt/p38 signalling pathways in chronic obstructive pulmonary disease: a network pharmacology study.
Article in Journal of molecular histology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Hei-Shun-Pian (HSP), prepared from Fuzi (the lateral root of Aconitum carmichaeli Debeaux) in traditional Chinese medicine (TCM) for the management of inflammatory and arthritic disorders. In this study, the therapeutic potential of Aconiti Lateralis Radix Praeparata (Heishunpian) was systematically investigated using an integrative network pharmacology, molecular docking, and in vivo experimental approach. The ameliorative effect of HSP was evaluated in an LPS-induced COPD mouse model. COPD-associated genes were retrieved from GeneCards, OMIM, and NCBI databases, and intersected with HSP-predicted targets from SwissTargetPrediction. Network analysis identified EGFR, IL6, JUN, AKT1, and PPARG as central regulatory nodes, with EGFR emerging as a key hub implicated in airway inflammation and epithelial remodelling. C57BL/6J mice were randomly assigned into six groups (n = 6 per group): normal control (NC); LPS (7.5 µg/50 µL saline); LPS + HSP (25 mg/kg); LPS + HCP (50 mg/kg); LPS + HCP (100 mg/kg); and HCP alone (100 mg/kg). Molecular docking demonstrated strong binding affinities of Songorine (- 8.4 kcal/mol) and 10-OH-Aconitine (- 7.9 kcal/mol) for EGFR, indicating potential suppression of EGFR-mediated inflammatory signalling. Collectively, these findings suggest that Heishunpian (HSP) exerts protective effects by modulating EGFR-driven inflammatory and oxidative pathways. COPD induction and treatment outcomes were assessed by evaluating body weight, lung index, oxidative stress parameters, fibrotic markers, cytokine profiles, lung histopathology, immunohistochemical analysis for PI3K and Akt, and qRT-PCR analysis. The antioxidative and anti-inflammatory activities of HSP were evidenced by the upregulation of the Nrf-2/NQO1/HO-1 axis and the suppression of Smad3/Akt/p38 signalling pathways.
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