Fucoxanthin Attenuates Behavior Deficits and Neuroinflammatory Response in 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine-Induced Parkinson's Disease in Mice

Background: Parkinson's disease (PD) is one of the foremost neurological disorders which is differentiated next to the progressive dopamine (DA) loss, especially in the area of substantia nigra pars compacta (SNpc). Aberrant neuroinflammation, as well as excessive reactive oxygen species (ROS) generation, have exposed to stimulate neuronal defeat in the gradual developing PD. The current study investigated whether fucoxanthin could attenuate the pathophysiology seen in an 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-mediated PD model. Materials and Methods: C57BL/6 mice received 30 mg/kg of MPTP (i.p.) every day for 5 consecutive days to establish PD, subsequently everyday treatment with fucoxanthin intended for 7 days. Intraperitoneal injection of MPTP, resulted in impaired motor functions, dopaminergic neuronal loss, decreased DA, Tyrosine hydroxylase (TH) levels, and microglial activation-mediated neuroinflammation. Results: Fucoxanthin administration ameliorated a-synuclein abnormal accumulation and motor impairment in MPTP-induced chronic PD mouse model. Our observed findings revealed that fucoxanthin administration reverses the MPTP-mediated decline of DA neuron, TH along with microglial activation predominantly in the SNpc region. The Western blot analysis exposed that fucoxanthin suppressed the expression patterns of proinflammatory cytokines following MPTP administration. Conclusion: In conclusion, Fucoxanthin exerts neuroprotective potential in opposition to MPTP-mediated PD mice through repressing a-synuclein expression, oxidative stress and gliosis, recommended that fucoxanthin might perform as a beneficial remedy toward PD amelioration.