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Brain Res Bull. 2018 May;139:9-15. doi: 10.1016/j.brainresbull.2018.01.017. Epub 2018 Feb 4.

Carvacrol prevents impairments in motor and neurochemical parameters in a model of progressive parkinsonism induced by reserpine.

Author information

1
Department of Physiology, Federal University of Sergipe, São Cristóvão, SE, Brazil.
2
Department of Biosciences, Federal University of Sergipe, Itabaiana, SE, Brazil.
3
Department of Biosciences, Federal University of São Paulo, Santos, SP, Brazil.
4
Department of Pharmacology, Federal University of São Paulo, São Paulo, SP, Brazil.
5
Department of Biosciences, Federal University of Sergipe, Itabaiana, SE, Brazil. Electronic address: joseronaldosantos@gmail.com.

Abstract

Parkinson's disease (PD) is a neurodegenerative disease characterized by a progressive degeneration of dopaminergic neurons in the substantia nigra pars compact (SNpc), with consequent depletion of dopamine in the striatum, which gives rise to the characteristic motor symptoms of PD. Although its etiology is unknown, several studies have suggested that oxidative stress plays a critical function in the pathophysiology of PD, and antioxidant agents could be helpful to slown down the dopaminergic neurodegeneration. Carvacrol (CA) is a phenolic monoterpene found in essential oils of many aromatic plants that presents antioxidant and neuroprotective effects. This study aimed to assess the effect of CA in a reserpine (RES)-induced rat model of PD. Male Wistar rats received 15 s.c. injections of 0.1 mg/kg RES or vehicle, every other day, concomitantly to daily i.p. injections of CA (12.5 or 25 mg/kg) or vehicle. Across the treatment, the animals were submitted to behavioral evaluation in the catalepsy test (performed daily), open field test (7th day) and assessment of vacuous chewing movements (12th, 20th and 30th days). Upon completion of behavioral tests, rats were perfused and their brains underwent tyrosine hydroxylase (TH) immunohistochemical analysis. Our results showed that CA (12.5 e 25 mg/kg) prevented the increase in catalepsy behavior and number of vacuous chewing movements, but failed to revert the decreased open-field locomotor activity induced by RES. In addition, CA in both doses prevented the decrease in TH immunostaining induced by RES in the SNpc and dorsal striatum. Taken together, our results suggest that CA shows a protective effect in a rat model of PD, preventing motor and neurochemical impairments induced by RES. Thus, the use of CA as a promising new strategy for the prevention and/or treatment of PD may be considered.

KEYWORDS:

Essential oils; Monoterpenes; Neuroprotective effect; Parkinsonism; Rat models

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