Although the etiology of
Parkinson's disease (PD) is poorly understood, studies in animal models revealed loss of
dopamine and the dopaminergic neurons harbouring the
neurotransmitter to be the principal cause behind this neuro-motor disorder.
Neuroinflammation with glial cell activation is suggested to play a significant role in dopaminergic neurodegeneration. Several biomolecules have been reported to confer dopaminergic neuroprotection in different animal models of PD, owing to their anti-inflammatory potentials.
Garcinol is a tri-isoprenylated
benzophenone isolated from Garcinia sp. and accumulating evidences suggest that this molecule could provide neuroprotection by modulating oxidative stress and
inflammation. However, direct evidence of dopaminergic neuroprotection by
garcinol in the pre-clinical model of PD is not yet reported. The present study aims to investigate whether administration of
garcinol in the
MPTP mouse model of PD may ameliorate the cardinal motor behavioural deficits and prevent the loss of dopaminergic neurons. As expected,
garcinol blocked the parkinsonian motor behavioural deficits which include akinesia,
catalepsy, and rearing anomalies in the mice model. Most importantly, the degeneration of dopaminergic cell bodies in the substantia nigra region was significantly prevented by
garcinol. Furthermore,
garcinol reduced the inflammatory marker,
glial fibrillary acidic protein, in the substantia nigra region. Since glial hyperactivation-mediated
inflammation is inevitably associated with the loss of dopaminergic neurons, our study suggests the anti-inflammatory role of
garcinol in facilitating dopaminergic neuroprotection in PD mice. Hence, in the light of the present study, it is suggested that
garcinol is an effective anti-parkinsonian agent to block motor behavioural deficits and dopaminergic neurodegeneration in PD.