Carvacrol Inhibits Expression of Transient Receptor Potential Melastatin 7 Channels and Alleviates Zinc Neurotoxicity Induced by Traumatic Brain Injury
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...
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MDPI AG
2022-11-01
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author | Minwoo Lee Song Hee Lee Seunghyuk Choi Bo Young Choi Sang Won Suh |
author_facet | Minwoo Lee Song Hee Lee Seunghyuk Choi Bo Young Choi Sang Won Suh |
author_sort | Minwoo Lee |
collection | DOAJ |
description | 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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spelling | doaj.art-472ed86c26c249219f5d6302793835da2023-11-24T08:34:31ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-11-0123221384010.3390/ijms232213840Carvacrol Inhibits Expression of Transient Receptor Potential Melastatin 7 Channels and Alleviates Zinc Neurotoxicity Induced by Traumatic Brain InjuryMinwoo Lee0Song Hee Lee1Seunghyuk Choi2Bo Young Choi3Sang Won Suh4Department of Physiology, Hallym University, College of Medicine, Chuncheon 24252, KoreaDepartment of Physiology, Hallym University, College of Medicine, Chuncheon 24252, KoreaDepartment of Physiology, Hallym University, College of Medicine, Chuncheon 24252, KoreaDepartment of Physical Education, Hallym University, Chuncheon 24252, KoreaDepartment of Physiology, Hallym University, College of Medicine, Chuncheon 24252, KoreaCarvacrol 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.https://www.mdpi.com/1422-0067/23/22/13840traumatic brain injuryzincneuronal deathtransient receptor potential melastatin 7carvacrol |
spellingShingle | Minwoo Lee Song Hee Lee Seunghyuk Choi Bo Young Choi Sang Won Suh Carvacrol Inhibits Expression of Transient Receptor Potential Melastatin 7 Channels and Alleviates Zinc Neurotoxicity Induced by Traumatic Brain Injury International Journal of Molecular Sciences traumatic brain injury zinc neuronal death transient receptor potential melastatin 7 carvacrol |
title | Carvacrol Inhibits Expression of Transient Receptor Potential Melastatin 7 Channels and Alleviates Zinc Neurotoxicity Induced by Traumatic Brain Injury |
title_full | Carvacrol Inhibits Expression of Transient Receptor Potential Melastatin 7 Channels and Alleviates Zinc Neurotoxicity Induced by Traumatic Brain Injury |
title_fullStr | Carvacrol Inhibits Expression of Transient Receptor Potential Melastatin 7 Channels and Alleviates Zinc Neurotoxicity Induced by Traumatic Brain Injury |
title_full_unstemmed | Carvacrol Inhibits Expression of Transient Receptor Potential Melastatin 7 Channels and Alleviates Zinc Neurotoxicity Induced by Traumatic Brain Injury |
title_short | Carvacrol Inhibits Expression of Transient Receptor Potential Melastatin 7 Channels and Alleviates Zinc Neurotoxicity Induced by Traumatic Brain Injury |
title_sort | carvacrol inhibits expression of transient receptor potential melastatin 7 channels and alleviates zinc neurotoxicity induced by traumatic brain injury |
topic | traumatic brain injury zinc neuronal death transient receptor potential melastatin 7 carvacrol |
url | https://www.mdpi.com/1422-0067/23/22/13840 |
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