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

    Hong, Dae Ki / Choi, Bo Young / Kho, A Ra / Lee, Song Hee / Jeong, Jeong Hyun / Kang, Beom Seok / Kang, Dong Hyeon / Park, Kyoung-Ha / Suh, Sang Won

    Cells

    2018  Volume 7, Issue 12

    Abstract: ... of reactive oxygen species and neurodegeneration. Carvacrol inhibits transient receptor potential melastatin 7 (TRPM7 ... we test whether carvacrol displays any neuroprotective effects after global cerebral ischemia (GCI), via ... of degenerating neurons, microglial activation, oxidative damage, and zinc translocation after GCI, via downregulation ...

    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.
    Language English
    Publishing date 2018-11-26
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2661518-6
    ISSN 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells7120231
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Carvacrol Attenuates Hippocampal Neuronal Death after Global Cerebral Ischemia via Inhibition of Transient Receptor Potential Melastatin 7

    Dae Ki Hong / Bo Young Choi / A Ra Kho / Song Hee Lee / Jeong Hyun Jeong / Beom Seok Kang / Dong Hyeon Kang / Kyoung-Ha Park / Sang Won Suh

    Cells, Vol 7, Iss 12, p

    2018  Volume 231

    Abstract: ... of reactive oxygen species and neurodegeneration. Carvacrol inhibits transient receptor potential melastatin 7 (TRPM7 ... we test whether carvacrol displays any neuroprotective effects after global cerebral ischemia (GCI), via ... of degenerating neurons, microglial activation, oxidative damage, and zinc translocation after GCI, via downregulation ...

    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.
    Keywords global cerebral ischemia ; carvacrol ; transient receptor potential melastatin 7 ; zinc ; neuronal death ; Biology (General) ; QH301-705.5
    Subject code 610
    Language English
    Publishing date 2018-11-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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