ArticleInternational journal of molecular sciences2022
Carvacrol Inhibits Expression of Transient Receptor Potential Melastatin 7 Channels and Alleviates Zinc Neurotoxicity Induced by Traumatic Brain Injury.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- TRPM7 kinase: a target for multimodal drug development in neurological disorders.Acta pharmacologica Sinica · 2026Review
- Phytochemistry and Bioactivities of Thymol and Carvacrol: Molecular Pathways, Metabolism, and Therapeutic Insights.Food science & nutrition · 2026Review
- Key Components of PPEO in Antagonizing Cerebral Ischemic Reperfusion Injury in Rats by Regulating Ferroptosis Through Arachidonic Acid Metabolic Pathway.Current issues in molecular biology · 2025Article
- Carvacrol Essential Oil as a Neuroprotective Agent: A Review of the Study Designs and Recent Advances.Molecules (Basel, Switzerland) · 2024Review
- Possible Combinatorial Utilization of Phytochemicals and Extracellular Vesicles for Wound Healing and Regeneration.International journal of molecular sciences · 2024Review
- Management of the Brain: Essential Oils as Promising Neuroinflammation Modulator in Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2024Review
- Article
- Therapeutic Potential of Myrtenal and Its Derivatives-A Review.Life (Basel, Switzerland) · 2023Review
- Pathophysiological Roles of Transient Receptor Potential (Trp) Channels and Zinc Toxicity in Brain Disease.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Carvacrol is a monoterpenoid phenol produced by aromatic plants such as oregano. Although the exact mechanism by which carvacrol acts has not yet been established, it appears to inhibit transient receptor potential melastatin 7 (TRPM7), which modulates the homeostasis of metal ions such as zinc and calcium. Several studies have demonstrated that carvacrol has protective effects against zinc neurotoxicity after ischemia and epilepsy. However, to date, no studies have investigated the effect of carvacrol on traumatic brain injury (TBI)-induced zinc neurotoxicity. In the present study, we investigated the therapeutic potential of carvacrol for the prevention of zinc-induced neuronal death after TBI. Rats were subjected to a controlled cortical impact, and carvacrol was injected at a dose of 50 mg/kg. Histological analysis was performed at 12 h, 24 h, and 7 days after TBI. We found that carvacrol reduced TBI-induced TRPM7 over-expression and free zinc accumulation. As a result, subsequent oxidative stress, dendritic damage, and neuronal degeneration were decreased. Moreover, carvacrol not only reduced microglial activation and delayed neuronal death but also improved neurological outcomes after TBI. Taken together, these findings suggest that carvacrol administration may have therapeutic potential after TBI by preventing neuronal death through the inhibition of TRPM7 expression and alleviation of zinc neurotoxicity.
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