The Kaohsiung Journal of Medical Sciences,
Год журнала:
2024,
Номер
40(8), С. 710 - 721
Опубликована: Июнь 5, 2024
Abstract
The
proinflammatory
properties
of
high‐mobility
group
box
protein
1
(HMGB1)
in
sepsis
have
been
extensively
studied.
This
study
aimed
to
investigate
the
impact
HMGB1
on
ferroptosis
and
its
molecular
mechanism
sepsis‐induced
acute
lung
injury
(ALI).
A
septic
mouse
model
was
established
using
cecal
ligation
puncture
method.
Blocking
resulted
improved
survival
rates,
reduced
injury,
decreased
levels
markers
(reactive
oxygen
species,
malondialdehyde,
Fe
2+
),
enhanced
antioxidant
enzyme
activities
(superoxide
dismutase
catalase)
mice.
In
addition,
knockdown
cellular
permeability,
markers,
raised
lipopolysaccharide
(LPS)‐stimulated
MLE‐12
cells.
Silencing
led
elevations
expressions
core‐regulators
LPS‐treated
cells,
such
as
solute
carrier
family
7
member
11
(SLC7A11),
3
A2
(SLC3A2),
glutathione
peroxidase
4.
Furthermore,
blocking
did
not
alter
ferroptosis,
oxidative
stress‐related
changes,
permeability
cells
that
were
pretreated
with
ferrostatin‐1
(a
inhibitor).
inhibition
also
elevated
nuclear
factor
erythroid
2‐related
2
(Nrf2)
downstream
targets,
heme
oxygenase‐1
(HO‐1)
NAD(P)H:
quinone
oxidoreductase
(NQO1)
tissues
from
Nrf2‐specific
inhibitor
ML385
reversed
effects
silencing
cell
Our
findings
indicated
restrains
stress,
thereby
alleviating
ALI
through
activation
Nrf2
signaling.
Cellular & Molecular Biology Letters,
Год журнала:
2024,
Номер
29(1)
Опубликована: Авг. 28, 2024
Stroke
is
a
type
of
acute
brain
damage
that
can
lead
to
series
serious
public
health
challenges.
Demonstrating
the
molecular
mechanism
stroke-related
neural
cell
degeneration
could
help
identify
more
efficient
treatment
for
stroke
patients.
Further
elucidation
factors
regulate
microglia
and
nuclear
factor
(erythroid-derived
2)-like
1
(Nrf1)
may
promising
strategy
treating
neuroinflammation
after
ischaemic
stroke.
In
this
study,
we
investigated
possible
role
pterostilbene
(PTS)
in
Nrf1
regulation
animal
models
ischaemia
Nanostructures
composed
of
liposomes
and
polydopamine
(PDA)
have
demonstrated
efficacy
as
carriers
for
delivering
plasmids,
effectively
alleviating
renal
cell
carcinoma.
However,
their
role
in
acute
kidney
injury
(AKI)
remains
unclear.
This
study
aimed
to
investigate
the
effects
plasmid-encoded
lncRNA-OIP5-AS1@PDA
nanoparticles
(POP-NPs)
on
ischemia/reperfusion
(RI/R)
explore
underlying
mechanisms.
RI/R
or
OGD/R
models
were
established
mice
HK-2
cells,
respectively.
In
vivo,
vector
POP-NPs
administered
(10
nmol,
IV)
48
h
after
treatment.
mouse
model,
OIP5-AS1
Nrf2/HO-1
expressions
down-regulated,
while
miR-410-3p
expression
was
upregulated.
treatment
reversed
RI/R-induced
tissue
injury,
restoring
altered
levels
blood
urea
nitrogen,
creatinine,
malondialdehyde,
inflammatory
factors
(IL-8,
IL-6,
TNF-α),
ROS,
apoptosis,
miR-410-3p,
well
suppressed
SOD
model
mice.
Similar
results
obtained
treated
with
POP-NPs.
Additionally,
mimics
could
reverse
cellular
models,
partially
counteracted
by
Nrf2
agonists.
The
binding
relationship
between
alongside
Nrf2,
has
been
substantiated
dual-luciferase
reporter
RNA
pull-down
assays.
revealed
that
can
attenuate
through
miR-410-3p/Nrf2
axis.
These
findings
lay
groundwork
future
targeted
therapeutic
approaches
utilizing
AKI.
Journal of Inflammation Research,
Год журнала:
2024,
Номер
Volume 17, С. 3383 - 3395
Опубликована: Май 1, 2024
Background:
Upon
uptake
by
stressed
cells,
functional
mitochondria
can
perform
their
normal
functions,
ultimately
enhancing
the
survival
of
host
cells.
However,
despite
promising
results
this
approach,
there
is
still
a
lack
understanding
specific
relationship
between
nerve
cells
and
mitochondria.
Methods:
Functional
(F-Mito)
were
isolated
from
bone
marrow-derived
mesenchymal
stem
(BMSCs).
The
ability
microglia
to
internalize
F-Mito
was
evaluated
using
middle
cerebral
artery
occlusion
(MCAO)
model
in
C57BL/6J
mice
an
oxygen-glucose
deprivation/reoxygenation
(OGD/R)
cell
model.
After
OGD/R
treatment,
temporal
dynamics
intracellular
reactive
oxygen
species
(ROS)
levels
examined.The
ROS
assessed
at
individual
level
MitoSOX,
Mitotracker,
HIF-1α
labeling.
Results:
Our
findings
indicate
that
exhibit
enhanced
mitochondrial
compared
astrocytes.
Furthermore,
internalized
reduced
levels.
Importantly,
we
found
response
following
ischemia
critical
regulator
internalization,
promoting
autophagy
might
reduce
Conclusion:
It
verified
derived
BMSCs
play
protective
role
ischemia-reperfusion
injury,
as
weakening
reduces
microglial
activation
alleviates
neuroinflammation.
Keywords:
neuroinflammation,
ROS,
cell,
HIF-1α,
ischemic
stroke
The Kaohsiung Journal of Medical Sciences,
Год журнала:
2024,
Номер
40(8), С. 710 - 721
Опубликована: Июнь 5, 2024
Abstract
The
proinflammatory
properties
of
high‐mobility
group
box
protein
1
(HMGB1)
in
sepsis
have
been
extensively
studied.
This
study
aimed
to
investigate
the
impact
HMGB1
on
ferroptosis
and
its
molecular
mechanism
sepsis‐induced
acute
lung
injury
(ALI).
A
septic
mouse
model
was
established
using
cecal
ligation
puncture
method.
Blocking
resulted
improved
survival
rates,
reduced
injury,
decreased
levels
markers
(reactive
oxygen
species,
malondialdehyde,
Fe
2+
),
enhanced
antioxidant
enzyme
activities
(superoxide
dismutase
catalase)
mice.
In
addition,
knockdown
cellular
permeability,
markers,
raised
lipopolysaccharide
(LPS)‐stimulated
MLE‐12
cells.
Silencing
led
elevations
expressions
core‐regulators
LPS‐treated
cells,
such
as
solute
carrier
family
7
member
11
(SLC7A11),
3
A2
(SLC3A2),
glutathione
peroxidase
4.
Furthermore,
blocking
did
not
alter
ferroptosis,
oxidative
stress‐related
changes,
permeability
cells
that
were
pretreated
with
ferrostatin‐1
(a
inhibitor).
inhibition
also
elevated
nuclear
factor
erythroid
2‐related
2
(Nrf2)
downstream
targets,
heme
oxygenase‐1
(HO‐1)
NAD(P)H:
quinone
oxidoreductase
(NQO1)
tissues
from
Nrf2‐specific
inhibitor
ML385
reversed
effects
silencing
cell
Our
findings
indicated
restrains
stress,
thereby
alleviating
ALI
through
activation
Nrf2
signaling.
