Journal of Inflammation Research,
Journal Year:
2025,
Volume and Issue:
Volume 18, P. 3937 - 3950
Published: March 1, 2025
Atherosclerosis
(AS)
is
a
chronic
inflammatory
disease
caused
by
the
dysregulation
of
lipid
metabolism.
It
has
been
established
that
oxidized
low-density
lipoprotein
(ox-LDL)-induced
macrophage
inflammation
and
ferroptosis
play
important
roles
in
AS.
However,
mechanism
which
ox-LDL
induces
macrophages
requires
further
investigation.
A
foam
cell
model
derived
from
ox-LDL-induced
was
constructed
to
study
its
action.
The
levels
interleukin
(IL)-6,
IL-1β,
tumor
necrosis
factor
(TNF)-α
were
evaluated
using
an
Enzyme-Linked
Immunosorbent
Assay
(ELISA).
Oil
Red
O
staining
used
detect
intracellular
accumulation
levels.
Lactate
dehydrogenase
(LDH),
malondialdehyde
(MDA),
reactive
oxygen
species
(ROS),
Fe2+
assessed.
Dual-luciferase
RNA-binding
protein
immunoprecipitation
(RIP)
experiments
validated
binding
relationship
between
microRNA
(miR)-214-3p
glutathione
peroxidase
4
(GPX4).
IL-6,
TNF-α
significantly
increased
macrophages,
accompanied
accumulation,
indicating
promotion
formation.
Additionally,
LDH,
MDA,
ROS,
Fe2+.
expression
miR-214-3p
positively
correlated
with
concentration
macrophages.
Treatment
inhibitor
reduces
responses,
RIP
confirmed
regulates
GPX4
transcription.
Silenced
reversed
effects
on
Low
also
promotes
induced
ox-LDL.
This
may
be
associated
miR-214-3p-induced
expression,
underscores
therapeutic
significance
targeting
addressing
Biomedicine & Pharmacotherapy,
Journal Year:
2023,
Volume and Issue:
166, P. 115415 - 115415
Published: Sept. 4, 2023
Iron,
as
an
essential
trace
element
for
the
organism,
is
vital
maintaining
organism's
health.
Excessive
iron
can
promote
reactive
oxygen
species
(ROS)
accumulation,
thus
damaging
cells
and
tissues.
Ferroptosis
a
novel
form
of
programmed
cell
death
distinguished
by
overload
lipid
peroxidation,
which
unique
from
autophagy,
apoptosis
necrosis,
more
studies
are
focusing
on
ferroptosis.
Recent
evidence
suggests
that
ferroptosis
associated
with
development
female
reproductive
disorders
(FRDs),
including
polycystic
ovary
syndrome
(PCOS),
premature
ovarian
insufficiency
(POI),
endometriosis
(EMs),
cancer
(OC),
preeclampsia
(PE)
spontaneous
abortion
(SA).
Pathways
genes
may
participate
in
processes
regulate
granulosa
proliferation
secretion,
oocyte
development,
reserve
function,
early
embryonic
placental
oxidative
stress.
However,
its
exact
mechanism
has
not
been
fully
revealed.
Therefore,
our
review
systematically
elaborates
occurrence
research
progress
FRDs,
view
to
providing
literature
references
clinical
targeting
-related
pathways
regulatory
factors
management
FRDs.
Ecotoxicology and Environmental Safety,
Journal Year:
2024,
Volume and Issue:
271, P. 115960 - 115960
Published: Jan. 16, 2024
Triphenyl
phosphate
(TPhP)
serves
as
a
major
organophosphorus
flame
retardant,
and
its
induced
neurodevelopmental
toxicity
has
attracted
widespread
attention,
but
the
mechanism
remains
unclear.
In
this
study,
we
involved
zebrafish
to
explore
new
of
TPhP
inducing
oxidative
stress
ferroptosis
promote
toxicity.
The
results
suggested
that
affected
embryonic
development,
reduced
number
neurons,
led
abnormal
neural
behavior
in
larvae.
also
ROS
accumulation,
activated
antioxidant
defense
signal
Nrf2
Keap1,
significantly
changed
activities
Acetylcholinesterase
(AChE),
Adenosine
triphosphatase
(ATPase)
glutathione
S-transferase
(GST).
addition,
zebrafish,
which
was
reflected
increase
Fe2+
content,
expression
GPX4
protein
genes
related
iron
metabolism
(gpx4a,
slc7a11,
acsl4b,
tfa,
slc40a1,
fth1b,
tfr2,
tfr1a,
tfr1b
ncoa4).
Astaxanthin
intervention
specifically
inhibited
levels,
reversed
SLC7A11
levels
thus
alleviating
by
TPhP.
partially
activity
AChE,
GST
neurodevelopmental-related
(gap43,
gfap,
neurog1
syn2a),
so
rescue
developmental
abnormalities
motor
disorders
More
interestingly,
mitochondrial
apoptosis-related
BAX,
anti-apoptotic
BCL-2,
Caspase3
Caspase9
altered
exposed
group,
could
be
intervention.
summary,
our
exposure
can
induce
ferroptosis,
thereby
causing
neurodevelopment
while
reverse
reduce
larvae
activating
Nrf2/Keap1/HO-1
signaling
pathway.
Chinese Medicine,
Journal Year:
2025,
Volume and Issue:
20(1)
Published: Jan. 15, 2025
Abstract
Background
Sepsis-induced
acute
lung
injury
(ALI)
is
a
severe
clinical
condition
accompanied
with
high
mortality.
Tangeretin,
which
widely
found
in
citrus
fruits,
has
been
reported
to
exert
antioxidant
and
anti-inflammatory
properties.
However,
whether
tangeretin
protects
against
sepsis-induced
ALI
the
potential
mechanisms
remain
unclear.
Methods
We
established
an
model
via
intraperitoneally
injected
5
mg/kg
lipopolysaccharides
(LPS)
for
12
h.
Tangeretin
was
applied
30
min
before
LPS
treatment.
Dexamethasone
(Dex)
used
as
positive
control.
Hematoxylin
eosin
(HE)
staining
protein
content
bronchoalveolar
lavage
fluid
(BALF)
were
determined
detect
degree
of
injury.
RNA-seq
also
explore
effect
on
ALI.
In
vitro,
RAW264.7
treated
Nrf2
siRNA,
expression
ferroptosis-associated
biomarkers,
including
glutathione
peroxidase
4
(GPX4)
prostaglandin-endoperoxide
synthase
2
(PTGS2)
assessed.
Glutathione
(GSH),
malondialdehyde
(MDA)
levels,
reactive
oxygen
species
(ROS)
inflammatory
factors
both
vivo
vitro.
Furthermore,
mice
inhibitor
(ML385)
verify
mechanism
inhibiting
ferroptosis.
Data
analyzed
using
one
way
analysis
variance
or
two-tailed
unpaired
t
tests.
Results
Our
study
demonstrated
that
significantly
alleviated
injury,
reversed
LPS-induced
reduction
GPX4
GSH,
mitigates
elevation
PTGS2
MDA
levels.
reduced
4-HNE
iron
Besides,
levels
LPS-stimulated
IL-6,
IL-1β
TNF-α
decreased
by
tangeretin.
bioinformatics
inhibited
response.
Mechanistically,
we
identified
GPX4-dependent
lipid
peroxidation
through
activation
Nrf2.
The
silence
abolished
inhibitory
oxidative
stress,
response
ferroptosis
cells.
Additionally,
all
protective
effects
inhibitor-treated
mice.
Conclusion
critical
contributing
promising
therapeutic
candidate,
effectively
upregulating
signaling
pathway.
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease,
Journal Year:
2023,
Volume and Issue:
1870(2), P. 166984 - 166984
Published: Dec. 6, 2023
Oxidative
stress
and
intestinal
inflammation
are
main
pathological
features
of
ulcerative
colitis
(UC).
Ferroptosis,
characterized
by
iron
accumulation
lipid
peroxidation,
is
closely
related
to
the
pathologic
process
UC.
16S
rRNA
sequencing
for
microbiota
analysis
gas
chromatography-mass
spectrometry
(GC-MS)
short-chain
fatty
acid
(SCFA)
contents
clearly
demonstrated
lower
amounts
butyrate-producing
bacteria
butyrate
in
mice.
However,
precise
mechanisms
sodium
(NaB)
treating
UC
remain
largely
unclear.
We
found
that
ferroptosis
occurred
models,
as
evidenced
inflammatory
response,
intracellular
level,
mitochondria
ultrastructural
observations
associated
protein
expression.
NaB
inhibited
colitis,
significantly
rescued
weight
loss
colon
shortening
mice
reduced
lesions
mitochondrial
damage.
Furthermore,
improved
barrier
integrity
markedly
suppressed
expression
pro-ferroptosis
proteins.
Conversely,
anti-ferroptosis
markers
including
nuclear
factor
erythroid-related
Factor
2
(Nrf2)
glutathione
peroxidase
4
(GPX4),
was
upregulated
with
treatment.
Moreover,
knockdown
Nrf2
reversed
anti-colitis
effect
NaB.
Taken
together,
exhibited
a
protective
ameliorating
experimental
through
Nrf2/GPX4
signaling
improving
integrity,
which
provides
novel
mechanism
prevention