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Cells 2018, 7(12), 231; https://doi.org/10.3390/cells7120231

Carvacrol Attenuates Hippocampal Neuronal Death after Global Cerebral Ischemia via Inhibition of Transient Receptor Potential Melastatin 7

1
Department of Physiology, College of Medicine, Hallym University, Chuncheon 24252, Korea
2
Division of Cardiovascular Diseases, Hallym University Sacred Heart Hospital, Anyang 14068, Korea
*
Author to whom correspondence should be addressed.
Received: 27 October 2018 / Revised: 21 November 2018 / Accepted: 23 November 2018 / Published: 26 November 2018
(This article belongs to the Special Issue Emerging Trends in Metal Biochemistry)
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Abstract

Over the last two decades, evidence supporting the concept of zinc-induced neuronal death has been introduced, and several intervention strategies have been investigated. Vesicular zinc is released into the synaptic cleft, where it then translocates to the cytoplasm, which leads to the production of reactive oxygen species and neurodegeneration. Carvacrol inhibits transient receptor potential melastatin 7 (TRPM7), which regulates the homeostasis of extracellular metal ions, such as calcium and zinc. In the present study, we test whether carvacrol displays any neuroprotective effects after global cerebral ischemia (GCI), via a blockade of zinc influx. To test our hypothesis, we used eight-week-old male Sprague–Dawley rats, and a GCI model was induced by bilateral common carotid artery occlusion (CCAO), accompanied by blood withdrawal from the femoral artery. Ischemic duration was defined as a seven-minute electroencephalographic (EEG) isoelectric period. Carvacrol (50 mg/kg) was injected into the intraperitoneal space once per day for three days after the onset of GCI. The present study found that administration of carvacrol significantly decreased the number of degenerating neurons, microglial activation, oxidative damage, and zinc translocation after GCI, via downregulation of TRPM7 channels. These findings suggest that carvacrol, a TRPM7 inhibitor, may have therapeutic potential after GCI by reducing intracellular zinc translocation. View Full-Text
Keywords: global cerebral ischemia; carvacrol; transient receptor potential melastatin 7; zinc; neuronal death global cerebral ischemia; carvacrol; transient receptor potential melastatin 7; zinc; neuronal death
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
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Hong, D.K.; Choi, B.Y.; Kho, A.R.; Lee, S.H.; Jeong, J.H.; Kang, B.S.; Kang, D.H.; Park, K.-H.; Suh, S.W. Carvacrol Attenuates Hippocampal Neuronal Death after Global Cerebral Ischemia via Inhibition of Transient Receptor Potential Melastatin 7. Cells 2018, 7, 231.

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