Evidence map›Paper›PMID 40947708›Full record

ArticleCombinatorial chemistry & high throughput screening2026

Exploring the Protective Effect and Potential Mechanism of Acutumidine on Myocardial Ischemia based on "Compound-Target-Pathway" Network.

Jia Shao, Rongrong Zheng, Meng Liu, Yingying Yu, Ling Luo, Jinxia Wei

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Article in Combinatorial chemistry & high throughput screening, 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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5 · Who and what money

Authors and funding

6 authors.

Jia ShaoDepartment of Pharmacy, Tianjin First Central Hospital, Tianjin, China.
Rongrong ZhengSchool of Chinese Materia Medica, Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Meng LiuSchool of Chinese Materia Medica, Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Yingying YuDepartment of Pharmacy, Logistical University of Chinese People's Armed Police, Tianjin, China.
Ling LuoSchool of Chinese Materia Medica, Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Jinxia WeiSchool of Chinese Materia Medica, Tianjin University of Traditional Chinese Medicine, Tianjin, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionMenispermi Rhizoma is a traditional Chinese medicine with significant Anti-Myocardial Ischemia (MI) effects. Acutumidine is a major alkaloid component of Menispermi Rhizoma. However, the effectiveness and potential mechanism of acutumidine in treating MI have been rarely studied. This research aims to explore the effect and mechanism of acutumidine on MI.

methodsThe function and mechanism of acutumidine in ameliorating MI were investigated via a comprehensive strategy of experimental evaluation, network pharmacology, and molecular docking. Firstly, the oxygen glucose deprivation (OGD) model of H9c2 cardiomyocytes was established to confirm the effects of acutumidine on MI. Then, network pharmacology was used to predict the potential targets and mechanisms of acutumidine in MI. The intersection targets between acutumidine and MI were acquired and used to construct a protein-protein interaction network. GO and KEGG enrichment analyses were performed using the Metascape database to reveal the probable mechanism of acutumidine on MI. Finally, the key potential targets of acutumidine were validated by molecular docking.

resultsCell experiments showed that acutumidine protected H9c2 cells against OGD injury by increasing SOD and GSH levels, decreasing LDH, CK, and MDA levels, and reducing apoptosis rates. Network pharmacology showed that the protective effect of acutumidine on MI was related to PI3K/AKT, HIF-1, and Ras signaling pathways. Molecular docking studies further showed that MAPK1, ESR1, EGFR, IGF1, and CASP3 are the core targets of acutumidine in treating MI. DISCUSSIONS: All research results suggested that acutumidine could inhibit oxidative stress and cell apoptosis.

conclusionsAcutumidine exhibits significant effects on MI, exerting pharmacological effects through multiple targets and pathways.

Indexed as

Myocardial IschemiaProtective AgentsAnimalsApoptosisCell LineCell SurvivalDose-Response Relationship, DrugImidazolesMolecular Docking SimulationMolecular StructureMyocytes, CardiacNetwork PharmacologyOxidative StressRatsSignal TransductionImidazolesmoxonidineProtective AgentsAcutumidinecell experimentmolecular dockingmyocardial ischemianetwork pharmacologyPI3K/AKT signaling pathway

Identifiers

PMID40947708

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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.