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@ARTICLE{Ali:285814,
author = {Ali, Mehak and Mehreen, Mehwish and Batool, Saima and Khan,
Shahrukh and Noor, Aneeqa and Mumtaz, Sara and Zafar, Saima},
title = {{C}hrysoeriol-{M}ediated {N}europrotection in {P}arkinson's
{D}isease in {M}ice: {T}argeting {A}poptosis, α-{S}ynuclein
{A}ccumulation, and {F}unctional {R}ecovery.},
journal = {Yale journal of biology and medicine},
volume = {99},
number = {1},
issn = {0044-0086},
address = {New Haven, Conn.},
publisher = {[Verlag nicht ermittelbar]},
reportid = {DZNE-2026-00350},
pages = {111 - 126},
year = {2026},
abstract = {Parkinson's disease (PD) is a neurodegenerative disorder
marked by the progressive loss of dopaminergic neurons in
the substantia nigra pars compacta, leading to significant
motor dysfunction. Current treatments stabilize dopamine
levels but fail to address underlying neuronal apoptosis,
highlighting the need for novel approaches. Although
chrysoeriol, a 3'-O-methoxy flavone and luteolin derivative,
is well-documented for its anti-cancer, anti-diabetic,
antioxidant, and anti-inflammatory properties, its
neuroprotective potential in PD, particularly in vivo,
remains largely unexplored. This study fills a critical gap
by being the first to systematically assess chrysoeriol's
neuroprotective effects in a PD mouse model. We evaluated
the effects of 5 mg/kg chrysoeriol administered
intraperitoneally (IP) for 14 days in an acute
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced
PD model. Behavioral tests showed notable recovery, as
chrysoeriol eliminated deficits in motor function,
coordination, and balance, as assessed by the pole test,
forced swim test, and tail suspension test. It also
mitigated exploratory and locomotor deficits in the open
field test, and the Y-maze test revealed improved spatial
and learning memory. Hematoxylin and eosin staining
indicated a significant reduction in neuronal damage across
key brain regions. qPCR analysis showed reduced
1-methyl-4-phenylpyridinium (MPP+)-induced toxicity,
downregulation of α-synuclein, and an improved Bcl-2/Bax
ratio. These findings suggest chrysoeriol may protect
against MPP+-induced apoptosis in mice, potentially via the
PI3K/Akt signaling pathway, and reduces mitochondrial damage
by downregulating α-synuclein.},
keywords = {Animals / Apoptosis: drug effects / alpha-Synuclein:
metabolism / Neuroprotective Agents: pharmacology /
Neuroprotective Agents: therapeutic use / Male / Parkinson
Disease: drug therapy / Parkinson Disease: metabolism / Mice
/ Mice, Inbred C57BL / Disease Models, Animal / Recovery of
Function: drug effects / Flavones: pharmacology /
Neuroprotection: drug effects / Dopaminergic Neurons: drug
effects / Dopaminergic Neurons: metabolism / BAX (Other) /
Bcl-2 (Other) / Neuroprotective (Other) / Parkinson’s
disease (Other) / chrysoeriol (Other) / α-Synuclein (Other)
/ alpha-Synuclein (NLM Chemicals) / Neuroprotective Agents
(NLM Chemicals) / Flavones (NLM Chemicals)},
cin = {AG Zerr},
ddc = {610},
cid = {I:(DE-2719)1440011-1},
pnm = {353 - Clinical and Health Care Research (POF4-353)},
pid = {G:(DE-HGF)POF4-353},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:41918512},
pmc = {pmc:PMC13023422},
doi = {10.59249/CTWM1697},
url = {https://pub.dzne.de/record/285814},
}