Key result
Angelicae Pubescentis Radix prolongs ventricular arrhythmia latency and reduces severity in an isoproterenol-induced rat model.
Why the study?
Does Angelicae Pubescentis Radix prevent arrhythmia and improve calcium cycling in an isoproterenol-induced rat model?
Does Angelicae Pubescentis Radix prevent arrhythmia and improve calcium cycling in an isoproterenol-induced rat model?
p-value: p=<0.001
Angelicae Pubescentis Radix demonstrates multi-target anti-arrhythmic potential in a rat model by improving cardiac electrical stability and restoring calcium handling.
Should not alter clinical practice; hypothesis-generating for APR in arrhythmia and requires human trials.
Objective This study aimed to elucidate the potential mechanisms by which Angelicae Pubescentis Radix (APR) prevents arrhythmia through the regulation of calcium channels, based on network pharmacology, molecular docking, and in vivo validation. Methods Active components of APR were screened from the TCMSP and PubChem databases under oral bioavailability (OB ≥ 30%) and drug-likeness (DL ≥ 0.18) criteria. Potential targets were predicted using SwissTargetPrediction and standardized using UniProt. Arrhythmia-related genes were collected from the GeneCards, OMIM, and TTD databases. Overlapping targets were identified for PPI network construction, GO/KEGG enrichment, and “component–target–pathway” network analysis. Core targets underwent molecular docking with key compounds. Furthermore, an isoproterenol (ISO)-induced arrhythmia rat model was established to evaluate the pharmacological effects of APR at different doses. Results A total of potential 340 putative APR-related targets were identified from network pharmacology analysis. Among the APR-derived active compounds, three with the highest network connectivity (Angelol G, O-acetylcolumbianetin, and nodakenin) were selected for molecular docking. In parallel, 902 arrhythmia-related genes were retrieved, yielding 24 overlapping targets, among which five hub genes (PIK3CA, CREBBP, NR3C1, SCN10A, and KCNA5) were identified. KEGG analysis revealed significant enrichment in calcium signaling, adrenergic signaling, and PI3K-Akt/cAMP pathways. Molecular docking demonstrated strong binding affinities between Angelol G, O-acetylcolumbianetin, and nodakenin to NR3C1 and SCN10A. In vivo , APR reduced VT/VF incidence and duration, prolonged arrhythmia latency, improved LVEF and FS, and decreased serum levels of CK-MB, LDH, and cTnI. APR also decreased p-CaMKII (Thr286) and increased p-PLN (Ser16/Thr17) and SERCA2a, indicating improved calcium cycling. Conclusion APR may exert anti-arrhythmic effects by targeting key regulatory nodes identified through network pharmacology, particularly PIK3CA, CREBBP, NR3C1, SCN10A, and KCNA5, and by exhibiting strong compound–target interactions in molecular docking. These network-predicted mechanisms were supported by in vivo findings, in which APR improved cardiac electrical stability, reduced myocardial injury, and restored Ca 2+ handling through the CaMKII–PLN–SERCA2a axis. Collectively, these results highlight APR’s multi-target cardioprotective potential and provide mechanistic evidence for its application in arrhythmia prevention.
No takes yet. Share an insight, caveat, or question.
Luo et al. (2026) studied Arrhythmia (n=24). Angelicae Pubescentis Radix (APR) vs. Vehicle (0.5% CMC-Na) was evaluated on Ventricular premature (VP) and ventricular tachycardia (VT) latency and survival time (p=<0.001). Angelicae Pubescentis Radix significantly prolonged ventricular premature and tachycardia latency and reduced arrhythmia severity in an isoproterenol-induced rat model.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: