Neuroscience Research Notes,
Год журнала:
2024,
Номер
7(2)
Опубликована: Май 19, 2024
Cerebral
neuroinflammation
has
emerged
as
a
significant
pathway
contributing
to
the
progression
of
Alzheimer's
disease
(AD)
pathology.
Research
implicates
NOD-like
receptor
family,
pyrin
domain
containing
3
(NLRP3)
inflammasome
complex,
initiating
caspase
1-mediated
maturation
interleukin-1
β
(IL-1β)
and
interleukin-18
(IL-18).
This
study
investigates
whether
chronic
cerebral
hypoperfusion
(CCH),
induced
via
permanent
bilateral
occlusion
common
carotid
arteries
(PBOCCA),
leads
cognitive
dysfunction
NLRP3
activation.
Twenty
male
Sprague
Dawley
(SD)
rats
underwent
PBOCCA
induce
CCH.
Two
weeks
post-surgery,
locomotor
Morris
water
maze
(MWM)
tests
were
conducted
examine
motor
functions,
spatial
learning,
memory,
respectively.
The
gene
expression
levels
cathepsin
B,
NLRP3,
an
apoptosis-associated
speck-like
protein
recruitment
(ASC),
caspase-1
analysed
using
real-time
PCR,
while
inflammatory
cytokines
estimated
ELISA
method.
Structural
damage
hippocampus
was
assessed
hematoxylin
eosin
(HE)
staining.
Escape
latencies
time
spent
in
specific
quadrants
significantly
increased
compared
sham-operated
animals.
There
no
notable
difference
activity
between
groups.
number
pyknotic
neurons
with
cytoplasmic
shrinkage
hippocampus.
Gene
ASC,
upregulated
group.
IL-1β,
IL-18,
interleukin-6
(IL-6),
amyloid-β
1-42
(Aβ
1-42)
elevated
group
relative
sham.
findings
confirm
induction,
dysfunction,
associated
AD
ischemia.
model
provides
valuable
tool
for
studying
neurodegenerative
including
AD.
ACS Medicinal Chemistry Letters,
Год журнала:
2023,
Номер
14(8), С. 1047 - 1048
Опубликована: Авг. 1, 2023
Provided
herein
are
novel
pyridazine
derivatives
as
NLRP3
inhibitors,
pharmaceutical
compositions,
use
of
such
compounds
in
treating
asthma,
COPD,
Parkinson's
disease,
and
Alzheimer's
processes
for
preparing
compounds.
Biochemistry and Biophysics Reports,
Год журнала:
2023,
Номер
36, С. 101559 - 101559
Опубликована: Окт. 19, 2023
Recently,
the
antioxidant
properties
of
natural
compound,
selenomethionine
(Se-Met),
have
been
recognized.
However,
its
effect
on
osteogenic
mineralization
Wnt/β-Catenin
pathway
under
conditions
oxidative
stress
and
inflammation
remain
unclear.This
study
utilized
tert-butyl
hydroperoxide
(TBHP)
to
simulate
inflammation.
Se-Met
was
then
subsequently
used
inhibit
these
effects
in
vitro.TBHP
induces
inflammatory
responses
by
increasing
expression
reactive
oxygen
species
NLRP3,
whereas
decreasing
GPX4,
thereby
inhibiting
viability
MC3T3-E1
cells.
TBHP
further
promotes
lipid
peroxidation
damages
ultrastructure
mitochondria.
Furthermore,
inhibits
levels
β-Catenin,
reducing
activity
Wnt
pathway,
which
turn
suppresses
differentiation
capacity.
Importantly,
significantly
alters
aforementioned
enhance
pathway-related
proteins
improving
capacity
cells.Se-Met
enhances
anti-inflammatory
cells
via
signaling
promote
osteogenesis.
Thus,
plays
a
crucial
role
field
bone
homeostasis,
presents
an
opportunity
for
future
development
novel
drugs
treating
osteoporosis
maintaining
stability.
detailed
preclinical
animal
studies
are
required
generate
solid
reliable
data
aid
this
development.
Neuroscience Research Notes,
Год журнала:
2024,
Номер
7(2)
Опубликована: Май 19, 2024
Cerebral
neuroinflammation
has
emerged
as
a
significant
pathway
contributing
to
the
progression
of
Alzheimer's
disease
(AD)
pathology.
Research
implicates
NOD-like
receptor
family,
pyrin
domain
containing
3
(NLRP3)
inflammasome
complex,
initiating
caspase
1-mediated
maturation
interleukin-1
β
(IL-1β)
and
interleukin-18
(IL-18).
This
study
investigates
whether
chronic
cerebral
hypoperfusion
(CCH),
induced
via
permanent
bilateral
occlusion
common
carotid
arteries
(PBOCCA),
leads
cognitive
dysfunction
NLRP3
activation.
Twenty
male
Sprague
Dawley
(SD)
rats
underwent
PBOCCA
induce
CCH.
Two
weeks
post-surgery,
locomotor
Morris
water
maze
(MWM)
tests
were
conducted
examine
motor
functions,
spatial
learning,
memory,
respectively.
The
gene
expression
levels
cathepsin
B,
NLRP3,
an
apoptosis-associated
speck-like
protein
recruitment
(ASC),
caspase-1
analysed
using
real-time
PCR,
while
inflammatory
cytokines
estimated
ELISA
method.
Structural
damage
hippocampus
was
assessed
hematoxylin
eosin
(HE)
staining.
Escape
latencies
time
spent
in
specific
quadrants
significantly
increased
compared
sham-operated
animals.
There
no
notable
difference
activity
between
groups.
number
pyknotic
neurons
with
cytoplasmic
shrinkage
hippocampus.
Gene
ASC,
upregulated
group.
IL-1β,
IL-18,
interleukin-6
(IL-6),
amyloid-β
1-42
(Aβ
1-42)
elevated
group
relative
sham.
findings
confirm
induction,
dysfunction,
associated
AD
ischemia.
model
provides
valuable
tool
for
studying
neurodegenerative
including
AD.
