4.5 Article

CARVACROL PROMOTES NEUROPROTECTION IN THE MOUSE HEMIPARKINSONIAN MODEL

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NEUROSCIENCE
卷 356, 期 -, 页码 176-181

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PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2017.05.013

关键词

carvacrol; dopamine; neuroprotection; TRP channels

资金

  1. Sao Paulo Research Foundation (FAPESP, Brazil) [2012/50880-4]
  2. National Council for Scientific and Technological Development (CNPq, Brazil)
  3. FAPESP fellowships
  4. Natural Sciences and Engineering Research Council of Canada (NSERC) [RGPIN-2014-06471, RGPIN-2016-04574]
  5. University of Toronto
  6. University of Sao Paulo
  7. Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [12/50880-4] Funding Source: FAPESP

向作者/读者索取更多资源

Carvacrol is a monoterpene that has been linked to neuroprotection in several animal models of neurodegeneration, including ischemia, epilepsy and traumatic neuronal injury. In this study, we investigated the effects of carvacrol (i.p.) upon the neurodegeneration induced by 6-hydroxydopamine unilateral intrastriatal injections in mice. We have also used the cylinder test to assess the behavioral effects of carvacrol in that model of Parkinson's disease, and immunoblots to evaluate the levels of caspase-3 and TRPM7, one of major targets of carvacrol. Behavioral testing revealed that carvacrol largely reduced the asymmetrical use of the forelimbs induced by unilateral 6-hydroxy-dopamine. Carvacrol dramatically reduced the loss of tyrosine hydroxylase immunostaining both in the substantia nigra and in the striatum that are typical of the model. Immunoblots for tyrosine hydroxylase confirmed this effect. Caspase-3 levels were very high after toxin injections, but carvacrol appeared to reduce them to control levels. Finally, TRPM7, observed by immunoblots, increased after 6-hydroxy-dopamine, suggesting the involvement of this cation channel in the ensuing neurodegenerative process. The present data suggest that carvacrol promotes a marked neuroprotection in the 6hydroxy-dopamine model of Parkinson's disease, possibly by its non-specific blocking effect upon TRPM7 channels. (C) 2017 IBRO. Published by Elsevier Ltd. All rights reserved.

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