Microgliosis and
inflammation are major wrongdoers in
cypermethrin-induced
Parkinsonism along with oxidative stress,
mitochondrial dysfunction and α-
synuclein aggregation.
Dopamine depletion could alter dendritic morphology, length and spine number in the striatum. Present study investigated the effect of
ibuprofen on the dendritic morphology, length and spine density in
cypermethrin PD model. Male pups were treated intraperitoneally with
cypermethrin during postnatal days followed by adulthood to induce
Parkinsonism using standard procedure along with controls. Subsets of animals were pre-treated with
ibuprofen 2 h prior to
cypermethrin treatment during adulthood. Standard methods were used to confirm
Parkinsonism/neuroprotection. Striatal dendritic morphology, length, spine number and expression of
synaptophysin and postsynaptic density protein-95 (PSD-95) along with the nigrostriatal pro-inflammatory and apoptotic
proteins were measured.
Cypermethrin induced Parkinsonian traits and attenuated the dendritic length, spine number and expression of
synaptophysin and PSD-95. While
cypermethrin increased the expression of interleukin-1β,
interleukin-4,
interferon-γ,
inducible nitric oxide synthase,
caspase-3,
caspase-9 and
B-cell lymphoma (Bcl)-xl
proteins, it attenuated Bcl-2 expression.
Ibuprofen normalized the changes in dendritic morphology, length, spine number and expression of
synaptophysin, PSD-95, and pro-inflammatory and apoptotic
proteins. Results demonstrate that
cypermethrin induces
inflammation and alters dendritic morphology, length and spine number, which are encountered by
ibuprofen.