The Mechanism of Baicalin in the Treatment of Mycoplasma Pneumoniae Pneumonia by Regulating NLRP3/Caspase-1 Signaling Pathway
Immunological Investigations,
Год журнала:
2025,
Номер
unknown, С. 1 - 13
Опубликована: Янв. 9, 2025
This
study
investigated
the
mechanism
of
baicalin
(BIA)
attenuating
inflammatory
response
and
lung
injury
in
mycoplasma
pneumoniae
pneumonia
(MPP)
mice.
MPP
mouse
models
were
established
then
treated
with
BIA,
azithromycin,
or
NLRP3
inflammasome
activator.
Lung
wet-to-dry
weight
(W/D)
ratio
weighed.
Serum
levels
MP-IgM,
C-reactive
protein
(CRP)
bronchoalveolar
lavage
fluid
(BALF)
detected
by
kits,
NLRP3/Caspase-1
pathway-related
Western
blot,
IL-1β,
IL-18,
IL-6
TNF-α
ELISA.
HE
staining
was
performed
to
detect
injury.
mice
showed
elevated
W/D
ratio,
upregulated
serum
MP-IgM
CRP
BALF
protein,
enhanced
levels,
which
reversed
BIA
azithromycin
treatment,
suggesting
that
attenuated
pulmonary
The
tissue
NLRP3,
cleaved
Caspase-1,Caspase-1,
GSDMD-N
GSDMD
raised
IL-1β
IL-18
changes
annulled
inhibited
pathway
activation.
activation
partially
abrogated
alleviative
effect
on
mitigates
inhibiting
Язык: Английский
Sinensetin attenuates LPS-induced acute pulmonary inflammation in mice and RAW264.7 cells by modulating NF-κB p65-mediated immune resistance and STAT3-mediated tissue resilience
International Immunopharmacology,
Год журнала:
2025,
Номер
148, С. 114101 - 114101
Опубликована: Янв. 18, 2025
Язык: Английский
Kirenol ameliorates endotoxin-induced acute lung injury by inhibiting the ERK and JNK phosphorylation–mediated NFκB pathway in mice
Inflammopharmacology,
Год журнала:
2025,
Номер
unknown
Опубликована: Март 4, 2025
Язык: Английский
TrxR1 is involved in the activation of Caspase-11 by regulating the oxidative-reductive status of Trx-1
Redox Biology,
Год журнала:
2024,
Номер
75, С. 103277 - 103277
Опубликована: Июль 20, 2024
Sepsis
is
a
common
complication
of
infections
that
significantly
impacts
the
survival
critically
patients.
Currently,
effective
pharmacological
treatment
strategies
are
lacking.
Auranofin,
known
as
an
inhibitor
Thioredoxin
reductase
(TrxR),
exhibits
anti-inflammatory
activity,
but
its
role
in
sepsis
not
well
understood.
Here,
we
demonstrate
significant
inhibitory
effect
Auranofin
on
cecal
ligation
and
puncture
(CLP)
mouse
model.
In
vitro,
inhibits
pyroptosis
triggered
by
Caspase-11
activation.
Further
investigations
reveal
inhibiting
TrxR1
suppresses
macrophage
induced
E.
coli,
while
TrxR2
does
exhibit
this
effect.
TrxR1,
functioning
reductase,
regulates
oxidative-reductive
status
Thioredoxin-1
(Trx-1).
Mechanistically,
modulation
Trx-1's
reductive
activity
may
be
involved
activation-induced
pyroptosis.
Additionally,
maintains
Trx-1
oxidized
state.
The
form
interacts
with
Caveolin-1
(CAV1),
regulating
outer
membrane
vesicle
(OMV)
internalization.
summary,
our
study
suggests
OMV
internalization
maintaining
Trx-1,
thereby
restricting
activation
alleviating
sepsis.
Язык: Английский