ArticlePharmaceutical biology2019
Allicin disrupts cardiac Cav1.2 channels via trafficking.
Article in Pharmaceutical biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The trial behind it
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- Mini-review: The health benefits and applications of allicin.Frontiers in pharmacology · 2025Review
- Article
- Therapeutic potentials of allicin in cardiovascular disease: advances and future directions.Chinese medicine · 2024Review
- Allicin promotes functional recovery in ischemic stroke via glutathione peroxidase-1 activation of Src-Akt-Erk.Cell death discovery · 2023Article
- High-expressed PTPN1 promotes tumor proliferation signature in human hepatocellular carcinoma.Heliyon · 2023Article
- Cellular Mechanisms Underlying the Cardioprotective Role of Allicin on Cardiovascular Diseases.International journal of molecular sciences · 2022Review
- Mecanismos moleculares de los efectos benéficos de la alicina sobre la enfermedad cardiovascular.Archivos de cardiologia de Mexico · 2022Review
- A review on plants and herbal components with antiarrhythmic activities and their interaction with current cardiac drugs.Journal of traditional and complementary medicine · 2020Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
contextAllicin is a potential antiarrhythmic agent. The antiarrhythmic properties of allicin rely on its blockade of various cardiac ion channels. The l-type calcium (Cav1.2) channel provides a pivotal substrate for cardiac electrophysiologic activities. The mechanism of allicin on Cav1.2 remains unclear.
objectiveThis study evaluated the potential of allicin on the synthesis and trafficking of Cav1.2 channels. MATERIALS AND
methodsPrimary cardiomyocytes (CMs) from neonatal Sprague-Dawley (SD) rats were exposed to allicin (0, 0.0001, 0.001, 0.01, 0.1, 1, 10, 100 μg/mL) for 24 and 48 h. The CellTiter-Glo assay was performed to measure CM viability. Western blot with grayscale analysis and confocal laser scanning microscopy were used to evaluate the effects of allicin on the synthesis and trafficking of Cav1.2 channel proteins in primary CMs.
resultsThere was no significant difference in apoptotic toxicity from the actual cell viability (p > 0.05) in any group (0, 0.0001, 0.001, 0.01, 0.1, 1, 10, 100 μg/mL allicin), except that viability in the 0.001 and 0.01 μg/mL groups at 24 h were significantly greater (137.37 and 135.96%) (p < 0.05). Western blot with grayscale analysis revealed no substantial inhibition by allicin of the synthesis of Cav1.2 proteins. Confocal laser scanning microscopy revealed trafficking dysfunction of Cav1.2 channels caused by allicin in primary CMs.
conclusionThis study is the first to demonstrate that allicin inhibits cardiac Cav1.2 channels by disrupting trafficking, possibly mediating its antiarrhythmic benefits. Therefore, allicin might serve as a new antiarrhythmic agent in the future.
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