Immunity Inflammation and Disease,
Journal Year:
2025,
Volume and Issue:
13(1)
Published: Jan. 1, 2025
Acute
lung
injury
(ALI),
one
of
the
most
severe
respiratory
system
diseases,
is
prevalent
worldwide.
Annexin
A1
(AnxA1)
an
important
member
annexin
superfamily,
known
for
its
wide
range
physiological
functions.
However,
potential
protective
effect
against
lipopolysaccharide
(LPS)-induced
ALI
remains
unclear.
Mice
were
divided
into
four
groups:
Sham,
LPS
+
vehicle,
0.1
μg
AnxA1,
and
0.5
AnxA1.
Lung
was
assessed
through
histopathology,
pulmonary
wet-to-dry
(W/D)
ratio,
cell
counting
bronchoalveolar
lavage
fluid
(BALF),
oxidative
stress
analysis,
noninvasive
function
testing.
Gene
protein
expression
levels
measured
using
RT-PCR,
ELISA,
western
blot
analysis.
AnxA1
alleviated
LPS-induced
by
protecting
tissue
from
damage,
reducing
wet/dry
weight
improving
impaired
function.
Interestingly,
administration
found
to
repress
infiltration
inflammatory
cells
decreasing
total
count,
neutrophils,
concentrations
in
(BALF).
mitigated
response
lowering
IL-1β,
IL-6,
TNF-α
BALF
mice.
Additionally,
attenuated
tissues
mice
restoring
activity
catalase
(CAT),
SOD,
glutathione
(GSH)
but
malondialdehyde
(MDA).
We
also
that
suppressed
activation
NLRP3
signaling
pathway.
Mechanistically,
activated
Nrf2/HO-1
pathway
while
preventing
NF-κB.
Collectively,
these
findings
suggest
alleviates
might
be
a
promising
novel
therapeutic
agent
ALI.
Pharmacognosy Magazine,
Journal Year:
2025,
Volume and Issue:
unknown
Published: April 14, 2025
Background
Pneumonia
is
a
serious
respiratory
illness
that
impacts
the
lungs,
leading
to
inflammation
and
fluid
accumulation
in
alveoli,
tiny
air
sacs
essential
for
gas
exchange.
Mycoplasma
pneumonia
severe
infection
caused
by
atypical
bacterium
pneumoniae
(MP).
Purpose
The
primary
objective
of
this
work
explore
therapeutic
effects
ferulic
acid
against
MP-infected
an
experimental
mice
model.
Methods
In
work,
BALB/c
were
subjected
100
µL
MP
challenge
via
nasal
drips
trigger
pneumonia.
then
administered
50
mg/kg
3
days.
After
experimentation,
lung
weight,
myeloperoxidase
(MPO),
nitric
oxide
(NO)
concentrations
assessed.
inflammatory
cytokines
oxidative
stress
biomarkers
analyzed
using
appropriate
diagnostic
kits.
total
cell
count
bronchoalveolar
lavage
(BAL)
deoxyribonucleic
(DNA)
concentration
lungs
assessed
mice.
histopathology
examination
was
conducted
evaluate
histological
abnormalities.
Results
administration
significantly
decreased
MPO,
NO
Ferulic
treatment
resulted
diminution
malondialdehyde
(MDA)
enhancement
glutathione
(GSH)
superoxide
dismutase
(SOD)
concentrations.
diminished
marker
MP-challenged
Furthermore,
reduced
DNA
content
counts
addition,
outcomes
indicated
significant
reduction
alveolar
damage
with
Conclusion
findings
confirm
salutary
properties
Consequently,
may
serve
as
effective
drug
candidate
treatment.
Journal of Toxicology and Environmental Health,
Journal Year:
2025,
Volume and Issue:
unknown, P. 1 - 10
Published: Jan. 8, 2025
Microcystin-LR
(MC-LR)
a
cyclic
toxin
produced
by
cyanobacterial
species
is
known
to
exert
detrimental
effects
on
various
organs,
including
lung.
Several
investigators
demonstrated
that
MC-LR
exerts
pulmonary
toxicity,
but
the
underlying
mechanisms
remain
unclear.
This
study
aimed
investigate
whether
exposure
MC-LR-induced
lung
inflammation
and
examine
mechanisms.
Thirty
specific
pathogen-free
(SPF)
male
mice
were
allocated
into
control
treatment
groups.
Mice
intraperitoneally
injected
with
physiological
saline
or
(20
μg/kg)
daily
for
total
of
21
days.
Our
findings
indicated
MC-LR-produced
histopathological
changes
in
tissue,
thickening
alveolar
walls
inflammatory
infiltration.
was
found
upregulate
mRNA
expression
levels
pro-inflammatory
cytokines
TNFα,
IL-6,
IL-1β,
IL-18.
Further,
significantly
elevated
proteins
associated
NF-κB/NLRP3
pathway
p-NF-κB,
NLRP3,
Caspase-1,
ASC.
The
activation
further
promoted
release
cytokine
IL-1β
cleavage
pyroptosis-associated
GSDMD
protein.
These
indicate
may
induce
promoting
cell
pyroptosis
via
pathway.
Immunity Inflammation and Disease,
Journal Year:
2025,
Volume and Issue:
13(1)
Published: Jan. 1, 2025
Acute
lung
injury
(ALI),
one
of
the
most
severe
respiratory
system
diseases,
is
prevalent
worldwide.
Annexin
A1
(AnxA1)
an
important
member
annexin
superfamily,
known
for
its
wide
range
physiological
functions.
However,
potential
protective
effect
against
lipopolysaccharide
(LPS)-induced
ALI
remains
unclear.
Mice
were
divided
into
four
groups:
Sham,
LPS
+
vehicle,
0.1
μg
AnxA1,
and
0.5
AnxA1.
Lung
was
assessed
through
histopathology,
pulmonary
wet-to-dry
(W/D)
ratio,
cell
counting
bronchoalveolar
lavage
fluid
(BALF),
oxidative
stress
analysis,
noninvasive
function
testing.
Gene
protein
expression
levels
measured
using
RT-PCR,
ELISA,
western
blot
analysis.
AnxA1
alleviated
LPS-induced
by
protecting
tissue
from
damage,
reducing
wet/dry
weight
improving
impaired
function.
Interestingly,
administration
found
to
repress
infiltration
inflammatory
cells
decreasing
total
count,
neutrophils,
concentrations
in
(BALF).
mitigated
response
lowering
IL-1β,
IL-6,
TNF-α
BALF
mice.
Additionally,
attenuated
tissues
mice
restoring
activity
catalase
(CAT),
SOD,
glutathione
(GSH)
but
malondialdehyde
(MDA).
We
also
that
suppressed
activation
NLRP3
signaling
pathway.
Mechanistically,
activated
Nrf2/HO-1
pathway
while
preventing
NF-κB.
Collectively,
these
findings
suggest
alleviates
might
be
a
promising
novel
therapeutic
agent
ALI.
