Biomedicine & Pharmacotherapy,
Год журнала:
2023,
Номер
165, С. 115057 - 115057
Опубликована: Июль 1, 2023
This
study
aimed
to
examine
whether
Biliverdin,
which
is
a
common
metabolite
of
haem,
can
alleviate
cerebral
ischemia
reperfusion
injury
(CIRI)
by
inhibiting
pyroptosis.
Here,
CIRI
was
induced
middle
artery
occlusion-reperfusion
(MCAO/R)
in
C57BL/6
J
mice
and
modelled
oxygen
glucose
deprivation/reoxygenation
(OGD/R)
HT22
cells,
it
treated
with
or
without
Biliverdin.
The
spatiotemporal
expression
GSDMD-N
infarction
volumes
were
assessed
immunofluorescence
staining
triphenyltetrazolium
chloride
(TTC),
respectively.
NLRP3/Caspase-1/GSDMD
pathway,
central
the
pyroptosis
process,
as
well
Nrf2,
A20,
eEF1A2
determined
Western-blots.
interactions
verified
using
dual-luciferase
reporter
assays,
chromatin
immunoprecipitation,
co-immunoprecipitation.
Additionally,
role
Nrf2/A20/eEF1A2
axis
modulating
neuroprotective
properties
Biliverdin
investigated
A20
gene
interference
(overexpression
and/or
silencing).
40
mg/kg
could
significantly
both
vivo
vitro,
promoted
activation
elevated
expression,
but
decreased
expression.
Nrf2
bind
promoter
thereby
transcriptionally
regulating
A20.
furthermore
interacted
through
its
ZnF4
domain
ubiquitinate
degrade
it,
leading
downregulation
eEF1A2.
Our
studies
have
also
demonstrated
that
either
knock-down
over-expression
blunted
protective
effect
Rescue
experiments
further
confirmed
regulate
NF-κB
pathway
via
axis.
In
summary,
our
demonstrates
ameliorates
findings
help
identify
novel
therapeutic
targets
for
treatment
CIRI.
Tetramethylpyrazine
(TMP)
has
been
confirmed
to
suppress
inflammation
in
endometriosis
(EMs).
Herein,
this
study
investigated
whether
and
how
TMP
affected
NLRP3
inflammasomes
oxidative
stress
EMs.
After
establishment
of
an
EMs
rat
model,
rats
were
treated
with
different
concentrations
TMP.
The
size
endometriotic
lesions
the
latency
frequency
torsion
recorded,
followed
by
measurement
relevant
indicators
(TNF-α,
IL-6,
IL-2,
IL-10,
MDA,
SOD,
GSH,
CAT,
ROS,
NLRP3,
ASC,
GSDMD,
caspase-1,
Nrf2,
HO-1).
experimentally
determined
that
treatment
markedly
decreased
improved
levels
inflammatory
proteins,
markers,
inflammasome,
pyroptotic
proteins
elevated
EMs,
all
which
reversed
upon
treatment.
Additionally,
activities
CAT
lowered
partly
abrogated
Furthermore,
downregulation
Nrf2
HO-1
was
counteracted
To
sum
up,
represses
excessive
stress,
inflammasome
activation,
pyroptosis
may
activate
Nrf2/HO-1
pathway.
Biomedicine & Pharmacotherapy,
Год журнала:
2023,
Номер
169, С. 115914 - 115914
Опубликована: Ноя. 24, 2023
Sepsis
is
a
life-threatening
systemic
inflammatory
response
syndrome
caused
by
the
host
imbalanced
to
infection.
Lung
injury
most
common
complication
of
sepsis
and
one
leading
causes
patient
death.
Pyroptosis
specific
programmed
cell
death
characterized
release
cytokines.
Appropriate
pyroptosis
can
reduce
tissue
damage
exert
protective
effect
against
infection
during
sepsis.
However,
overactivated
results
in
massive
death,
septic
shock,
multiple
organ
dysfunction
syndrome,
even
an
increased
risk
secondary
Recent
studies
suggest
that
interact
with
cross-regulate
other
types
programs
establish
complex
network
which
participates
occurrence
development
lung
injury.
This
review
will
focus
on
interactions
between
including
apoptosis,
necroptosis,
PANoptosis,
NETosis,
autophagy,
ferroptosis,
summarize
role
sepsis-induced
injury,
discuss
potential
therapeutic
strategies
targeting
treatment.
Antioxidants,
Год журнала:
2024,
Номер
13(8), С. 1012 - 1012
Опубликована: Авг. 20, 2024
Oxidative
stress
(OS)
is
a
key
factor
in
the
generation
of
various
pathophysiological
conditions.
Nuclear
erythroid
2
(NF-E2)-related
(Nrf2)
major
transcriptional
regulator
antioxidant
reactions.
Heme
oxygenase-1
(HO-1),
gene
regulated
by
Nrf2,
one
most
critical
cytoprotective
molecules.
In
recent
years,
Nrf2/HO-1
has
received
widespread
attention
as
regulatory
pathway
for
intracellular
defense
against
oxidative
stress.
It
considered
potential
target
treatment
inflammatory
bowel
disease
(IBD).
This
review
highlights
mechanism
action
and
therapeutic
significance
IBD
complications
(intestinal
fibrosis
colorectal
cancer
(CRC)),
well
phytochemicals
targeting
IBD.
The
results
suggest
that
effects
on
mainly
involve
following
aspects:
(1)
Controlling
to
reduce
intestinal
inflammation
injury;
(2)
Regulation
flora
repair
mucosal
barrier;
(3)
Prevention
ferroptosis
epithelial
cells.
However,
due
complex
role
Nrf2/HO-1,
more
nuanced
understanding
exact
mechanisms
involved
way
forward
future.
Cell Death Discovery,
Год журнала:
2024,
Номер
10(1)
Опубликована: Май 24, 2024
Abstract
Ferroptosis
is
a
novel
form
of
programmed
cell
death
which
can
exacerbate
lung
injury
in
septic
acute
respiratory
distress
syndrome
(ARDS).
Alveolar
macrophages,
crucial
innate
immune
cells,
play
pivotal
role
the
pathogenesis
ARDS.
Ferritinophagy
process
ferritin
degradation
mediated
by
nuclear
receptor
coactivator
4
(NCOA4)
releases
large
amounts
iron
ions
thus
promoting
ferroptosis.
Recent
evidence
revealed
that
inhibiting
macrophage
ferroptosis
effectively
attenuate
pulmonary
inflammatory
injury.
Melatonin
(MT),
an
endogenous
neurohormone,
has
antioxidant
and
anti-inflammatory
effects
reduce
However,
it
not
clear
whether
MT’s
protective
effect
related
to
inhibition
ferritinophagy.
Our
vitro
experiments
demonstrated
MT
decreased
intracellular
malondialdehyde
(MDA),
Fe
2+
,
lipid
peroxidation
levels,
increased
glutathione
(GSH)
levels
proliferation,
upregulated
peroxidase
(GPX4)
heavy
chain
1
(FTH1)
protein
LPS-treated
macrophages.
Mechanistically,
antiferroptotic
on
macrophages
was
significantly
compromised
overexpression
NCOA4.
vivo
alleviated
expression
NCOA4
FTH1
alveolar
mice.
Furthermore,
improved
mitigated
damage
tissue,
ultimately
increasing
survival
rates
These
findings
indicate
inhibit
NCOA4-mediated
ferritinophagy
manner,
thereby
ameliorating
Journal of Inflammation Research,
Год журнала:
2024,
Номер
Volume 17, С. 3801 - 3813
Опубликована: Июнь 1, 2024
Abstract:
Acute
lung
injury
(ALI)
manifests
through
harm
to
the
capillary
endothelium
and
alveolar
epithelial
cells,
arising
from
a
multitude
of
factors,
leading
scattered
interstitial
alterations,
pulmonary
edema,
subsequent
acute
hypoxic
respiratory
insufficiency.
(ALI),
along
with
its
more
serious
counterpart,
distress
syndrome
(ARDS),
carry
fatality
rate
that
hovers
around
30–
40%.
Its
principal
pathological
characteristic
lies
in
unchecked
inflammatory
reaction.
Currently,
main
strategies
for
treating
ALI
are
alleviation
inflammation
prevention
failure.
Concerning
etiology
ALI,
NLRP3
Inflammasome
is
essential
body's
innate
immune
response.
The
composition
this
inflammasome
complex
includes
NLRP3,
pyroptosis
mediator
ASC,
pro-caspase-1.
Recent
research
has
reported
response
centered
on
inflammasomes
plays
key
part
may
hence
be
prospective
candidate
therapeutic
intervention.
In
review,
we
present
an
overview
ailment
characteristics
constitution
operation
within
framework.
We
also
explore
targeting
combat
injury.
Keywords:
injury,
inflammasome,
caspase-1,
IL-1β,
IL-18
International Immunopharmacology,
Год журнала:
2023,
Номер
116, С. 109734 - 109734
Опубликована: Янв. 25, 2023
Kirenol
is
a
bioactive
substance
isolated
from
Herba
Siegesbeckiae.
Although
the
anti-inflammatory
activity
of
kirenol
has
been
well
documented,
its
role
in
autophagy
remains
unknown.
The
present
study
aimed
to
investigate
protective
on
inflammation
challenged
by
lipopolysaccharide
(LPS)
acute
lung
injury
(ALI)
cell
and
mouse
models
unravel
underlying
mechanisms,
with
particular
focus
autophagy.
For
this
purpose,
an
ALI
were
established,
effects
expression
molecules
related
examined.
results
revealed
that
could
significantly
inhibit
inflammatory
cytokines
secretion
cells
mice
injured
LPS;
effect
may
be
attributed
enhanced
as
evidenced
up-regulation
LC3-II
down-regulation
p62
both
vitro
vivo.
Phosphorylated
AMPK
ULK1
increased,
while
phosphorylated
mTOR
decreased
kirenol-treated
model.
Moreover,
inhibition
using
inhibitor
or
3-MA
chloroquine
(CQ)
reversed
autophagy-enhancement
exposure
vitro,
indicating
enhance
activating
AMPK-mTOR-ULK1
pathway.
RNA
sequencing
suggested
was
strongly
biological
functions
response
signaling
Further
vivo
model
studies
demonstrated
against
inflammation,
such
improved
histopathology,
edema,
leukocyte
infiltration
abolished
3-MA.
These
findings
implicate
can
LPS-induced
via
Molecules,
Год журнала:
2023,
Номер
28(3), С. 967 - 967
Опубликована: Янв. 18, 2023
The
purpose
of
this
work
was
to
illustrate
the
effect
processing
with
vinegar
on
saikosaponins
Bupleurum
chinense
DC.
(BC)
and
protective
effects
saikosaponin
A
(SSA),
b1
(SSb1),
b2
(SSb2),
D
(SSD)
in
lipopolysaccharide
(LPS)-induced
acute
lung
injury
(ALI)
mice.
We
comprehensively
evaluated
anti-inflammatory
potential
mechanisms
SSA,
SSb1,
SSb2,
SSD
through
an
LPS-induced
ALI
model
using
intratracheal
injection.
results
showed
that
significantly
decreased
pulmonary
edema;
reduced
levels
IL-6,
TNF-α,
IL-1β
serum
tissues;
alleviated
pathological
damage;
genes
expression
NF-κB/TLR4-related
proteins.
Interestingly,
they
were
similar
structure,
but
SSb2
had
a
better
at
same
dose,
according
principal
component
analysis.
These
findings
indicated
it
may
not
have
been
comprehensive
only
use
SSA
as
indicators
evaluate
quality
BC,
especially
contents
SSb1
vinegar-processed
BC
increased.