This study investigated the effects of curcumin on nigrostriatal dopaminergic (DA) neurons and glial response in 6-hydroxydopamine (6-OHDA) hemiparkinsonian mice. Following unilateral intrastriatal 6-OHDA injection, mice were daily injected with curcumin for seven days, beginning on the day of lesion. Seven days after 6-OHDA lesioning, sections from the striatum and the substantia nigra pars compacta (SNpc) were collected and immunohistochemically stained for DA neurons and reactive glia. Curcumin decreased 6-OHDA-induced loss of nigral tyrosine hydroxylase-immunoreactive (TH-IR) neurons and striatal TH-IR fibers. The neuroprotection was coincided with a significant attenuation of microglial and astroglial reaction in the SNpc and the striatum. These results suggest that the neuroprotective effects of curcumin in 6-OHDA-lesioned mice may be mediated through its anti-inflammatory properties or direct protection on nigral DA neurons, thereby reducing neuronal injury-induced glial activation.
Degeneration of dopaminergic (DA) axons in the striatum triggers upregulation of striatal trophic activity and striatal DA neuronal number in animal models of Parkinson's disease (PD). The present study investigated the effects of 17beta-estradiol (E2) on brain-derived neurotrophic factor (BDNF) expression and the density of DA neurons in the striatum of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model in correlation with nigrostriatal DA innervation. Adult male C57Bl/6 mice were treated with E2 or vehicle for 11 days. Following 5 days of E2 or vehicle pretreatment, animals were injected with MPTP on day 6. On day 11, all mice were sacrificed, and the striatum were collected and processed for tyrosine hydroxylase (TH) and BDNF immunohistochemistry. Striatal TH-immunoreactive (IR) neurons were counted. Extent of DA innervation and BDNF expression in the striatum were assessed by measuring optical density of TH and BDNF immunoreactivity, respectively. Pretreatment with E2 partially prevented DA denervation and decreased striatal BDNF upregulation triggered by MPTP, but maintained the density of striatal TH-IR neurons to that observed in MPTP group. These findings suggest that estrogen protection of nigrostriatal DA axons against MPTP as well as preservation of the striatal TH-IR cell density in MPTP/E2 mice may be not mediated by BDNF.
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