Diabetes,
Journal Year:
2024,
Volume and Issue:
73(9), P. 1513 - 1526
Published: June 13, 2024
Diabetic
encephalopathy
(DE)
is
a
severe
complication
of
the
central
nervous
system
associated
with
diabetes.
In
this
study,
we
investigated
regulatory
role
mammalian
target
rapamycin
(mTOR)
on
nuclear
factor
κB
(NF-κB)
in
mice
DE,
and
neuroprotective
effect
therapeutic
mechanisms
luteolin,
natural
flavonoid
compound
anti-inflammatory,
antioxidant,
properties.
The
results
indicated
that
treatment
luteolin
improved
degree
cognitive
impairment
DE.
It
also
decreased
levels
phosphorylated
mTOR,
NF-κB,
histone
deacetylase
2
(HDAC2)
increased
expression
brain-derived
neurotrophic
synaptic-related
proteins.
Furthermore,
protein-protein
interaction
Gene
Ontology
analysis
revealed
was
involved
network
HDAC2
through
mTOR/NF-κB
signaling
cascade.
Our
bioinformatics
molecular
docking
may
directly
HDAC2,
as
an
inhibitor,
to
alleviate
complementing
inhibition.
Analysis
luteolin's
proteins
their
interactions
suggest
cognition.
conclusion,
tau
hyperphosphorylation
are
regulated
by
cascade
found
reverse
these
effects,
demonstrating
its
protective
Archives of Gerontology and Geriatrics,
Journal Year:
2024,
Volume and Issue:
129, P. 105684 - 105684
Published: Nov. 12, 2024
There
is
a
lack
of
information
on
the
molecular
mechanisms
by
which
steroid
hormones
(testosterone,
estrogen,
and
progesterone)
regulate
cognitive
impairment.
Thus,
we
aimed
to
identify
protective
effects
function.
Diabetes,
Journal Year:
2024,
Volume and Issue:
73(9), P. 1513 - 1526
Published: June 13, 2024
Diabetic
encephalopathy
(DE)
is
a
severe
complication
of
the
central
nervous
system
associated
with
diabetes.
In
this
study,
we
investigated
regulatory
role
mammalian
target
rapamycin
(mTOR)
on
nuclear
factor
κB
(NF-κB)
in
mice
DE,
and
neuroprotective
effect
therapeutic
mechanisms
luteolin,
natural
flavonoid
compound
anti-inflammatory,
antioxidant,
properties.
The
results
indicated
that
treatment
luteolin
improved
degree
cognitive
impairment
DE.
It
also
decreased
levels
phosphorylated
mTOR,
NF-κB,
histone
deacetylase
2
(HDAC2)
increased
expression
brain-derived
neurotrophic
synaptic-related
proteins.
Furthermore,
protein-protein
interaction
Gene
Ontology
analysis
revealed
was
involved
network
HDAC2
through
mTOR/NF-κB
signaling
cascade.
Our
bioinformatics
molecular
docking
may
directly
HDAC2,
as
an
inhibitor,
to
alleviate
complementing
inhibition.
Analysis
luteolin's
proteins
their
interactions
suggest
cognition.
conclusion,
tau
hyperphosphorylation
are
regulated
by
cascade
found
reverse
these
effects,
demonstrating
its
protective
