Journal of Orthopaedic Surgery and Research,
Год журнала:
2024,
Номер
19(1)
Опубликована: Март 11, 2024
Abstract
Background
Cholesterol
(CHO)
is
an
essential
component
of
the
body.
However,
high
CHO
levels
in
body
can
damage
bone
mass
and
promote
osteoporosis.
accumulation
cause
osteoblast
apoptosis,
which
has
a
negative
effect
on
formation.
The
pathogenesis
osteoporosis
complicate
process
that
includes
oxidative
stress,
endoplasmic
reticulum
(ER)
inflammation.
Geniposide
(GEN)
natural
compound
with
anti-osteoporotic
effect.
roles
GEN
osteopathogenesis
are
still
unclear.
Our
previous
studies
demonstrated
could
reduce
osteoblasts
activation
ER
stress
osteoblasts.
molecular
mechanism
inhibiting
CHO-induced
apoptosis
needs
to
be
further
investigated.
Methods
MC3T3-E1
cells
were
treated
osteogenic
induction
medium
(OIM).
Ethanol-solubilized
cholesterol
(100
µM)
was
used
as
stimulator,
10
µM
25
geniposide
added
for
treatment.
alterations
protein
expression
detected
by
western
blot,
cell
analyzed
flow
cytometer.
Results
promoted
activating
osteoblasts,
while
alleviated
reduced
GLP-1R/ABCA1
pathway.
Inhibition
ABCA1
or
GLP-1R
eliminate
protective
activity
against
apoptosis.
Conclusion
mediating
bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2024,
Номер
unknown
Опубликована: Фев. 21, 2024
ABSTRACT
Microglia-driven
neuroinflammation
plays
an
important
role
in
the
development
of
Alzheimer’s
disease
(AD).
Microglia
activation
is
accompanied
by
formation
and
chronic
maintenance
TLR4
inflammarafts,
defined
as
enlarged
cholesterol-rich
lipid
rafts
serving
assembly
platform
for
dimers
complexes
other
inflammatory
receptors.
The
secreted
apoA-I
binding
protein
(APOA1BP
or
AIBP)
binds
selectively
targets
cholesterol
depletion
machinery
to
inflammaraft
expressing
inflammatory,
but
not
homeostatic
microglia.
Here
we
demonstrated
that
amyloid-beta
(Aβ)
induced
inflammarafts
microglia
vitro
brain
APP/PS1
mice.
Mitochondria
Apoa1bp
-/-
were
hyperbranched
cupped,
which
was
increased
ROS
dilated
ER.
size
number
Aβ
plaques
neuronal
cell
death
significantly
increased,
animal
survival
decreased
compared
female
These
results
suggest
AIBP
exerts
control
mitochondrial
dynamics
a
protective
AD
associated
oxidative
stress
neurodegeneration.
Ankara Üniversitesi Veteriner Fakültesi Dergisi,
Год журнала:
2024,
Номер
71(4), С. 395 - 406
Опубликована: Март 8, 2024
This
research
focused
on
exploring
the
therapeutic
impact
of
black
garlic
ethanol
extract
(BGE)
brain
tissue
rats
exposed
to
acrylamide
(ACR).
Twenty-four
female
were
divided
into
four
groups.
Rats
in
control
group
given
1
ml
saline
by
oral
gavage
for
14
days.
The
BG
received
5
mg/200
g
BGE
a
daily
basis.
ACR
was
administered
40
mg/kg
daily.
BGE+ACR
both
and
Brain
samples
collected
at
study's
conclusion
histopathological,
immunohistochemical,
biochemical
analyses.
Hematoxylin-eosin
staining
performed
examine
general
structure
tissue.
Erk1/2,
p-ERK1/2,
c-fos
analyzed
immunohistochemically;
Bcl-2,
Caspase-3,
ATF6,
CREB,
NfkB-p65
protein
levels
Western
blotting;
MDA,
SOD,
CAT,
GSH,
TNF-α,
IL-1β,
IL-6
activities
using
ELISA
kits.
It
determined
that
application
raised
c-Fos,
NfkB-p65,
caspase-3,
IL-6,
IL-1-β,
supplementation
decreased
this
increase.
exposure
caused
decrease
SOD
expressions,
prevented
or
increased
decrease.
Based
findings
obtained,
it
can
be
said
has
antioxidative
anti-inflammatory
effects,
prevents
cell
damage,
positive
effects
apoptosis
rat
Journal of Orthopaedic Surgery and Research,
Год журнала:
2024,
Номер
19(1)
Опубликована: Март 11, 2024
Abstract
Background
Cholesterol
(CHO)
is
an
essential
component
of
the
body.
However,
high
CHO
levels
in
body
can
damage
bone
mass
and
promote
osteoporosis.
accumulation
cause
osteoblast
apoptosis,
which
has
a
negative
effect
on
formation.
The
pathogenesis
osteoporosis
complicate
process
that
includes
oxidative
stress,
endoplasmic
reticulum
(ER)
inflammation.
Geniposide
(GEN)
natural
compound
with
anti-osteoporotic
effect.
roles
GEN
osteopathogenesis
are
still
unclear.
Our
previous
studies
demonstrated
could
reduce
osteoblasts
activation
ER
stress
osteoblasts.
molecular
mechanism
inhibiting
CHO-induced
apoptosis
needs
to
be
further
investigated.
Methods
MC3T3-E1
cells
were
treated
osteogenic
induction
medium
(OIM).
Ethanol-solubilized
cholesterol
(100
µM)
was
used
as
stimulator,
10
µM
25
geniposide
added
for
treatment.
alterations
protein
expression
detected
by
western
blot,
cell
analyzed
flow
cytometer.
Results
promoted
activating
osteoblasts,
while
alleviated
reduced
GLP-1R/ABCA1
pathway.
Inhibition
ABCA1
or
GLP-1R
eliminate
protective
activity
against
apoptosis.
Conclusion
mediating
