Inhibition of N6-methyladenosine methylation of ASC by berberine ameliorates pyroptosis of renal tubular epithelial cells in acute kidney injury
Cellular Signalling,
Год журнала:
2025,
Номер
unknown, С. 111732 - 111732
Опубликована: Март 1, 2025
Acute
kidney
injury
(AKI)
lacks
a
definitive
therapeutic
approach
beyond
supportive
care.
One
significant
pathological
mechanism
involves
the
regulated
death
of
tubular
epithelial
cells;
however,
regulatory
mechanisms
underlying
this
cell
pathway
require
further
investigation.
The
N6-methyladenosine
(m6A)
modification,
recognized
as
most
prevalent
modification
in
eukaryotes,
plays
critical
role
processes
associated
with
AKI.
Here,
study
investigates
association
between
methyltransferase-like
3
(METTL3)
and
pyroptosis
mice
folic
acid
(FA)-induced
Both
vitro
vivo
experiments
have
confirmed
that
METTL3
AKI
progression,
correlating
renal
inflammation.
Moreover,
RNA
immunoprecipitation
quantitative
PCR
(RIP-qPCR)
analysis
demonstrated
METTL3-mediated
m6A
methylation
occurred
mRNA
Apoptosis-associated
speck-like
protein
containing
CARD
(ASC)
H2O2-induced
(TCMK-1)
cells.
Notably,
knockdown
resulted
reduced
ASC
expression,
decreased
release
inflammatory
factors,
pyroptosis.
In
addition,
we
verified
inhibitory
effect
berberine
hydrochloride,
monomer
used
traditional
Chinese
medicine,
on
expression.
We
also
ameliorated
FA-induced
TCMK-1
cells
by
inhibiting
modulating
ASC/caspase-1/Gasdermin
D
axis.
These
findings
provide
insights
into
targeted
therapies
drug
development
for
Язык: Английский
Mechanistic Insights into T-2 Toxin-Induced Thymic Epithelial Cell Injury and Immunotoxicity via the ROS-NF-κB-NLRP3 Signaling Axis
Journal of Agricultural and Food Chemistry,
Год журнала:
2025,
Номер
unknown
Опубликована: Май 19, 2025
Thymic
epithelial
cells
(TECs)
are
critical
for
thymic
structure
and
function,
yet
the
impact
of
T-2
toxin
(T-2)
on
TECs
related
molecular
pathways
remains
unclear.
This
study
sheds
light
mechanisms
T-2-induced
TEC
damage,
focusing
ROS-NF-κB-NLRP3
signaling
axis.
The
in
vivo
vitro
analyses
suggest
that
induces
injury
through
ROS-driven
NLRP3
inflammasome
activation,
NF-κB
signaling,
inflammation,
apoptosis.
Molecular
docking
analysis
verified
binding
to
components
involved
oxidative
stress,
inflammatory
pathways,
These
findings
were
further
supported
by
therapeutic
interventions
targeting
ROS
NLRP3.
N-acetylcysteine
(NAC)
effectively
reduced
levels,
suppressed
inhibited
mitigated
inflammation
apoptosis,
effects
mirrored
inhibitor
MCC950,
emphasizing
role
ROS-mediated
activation
damage.
Concurrently,
inhibition
apoptosis
MTEC1
cells,
pivotal
function
axis
pathogenesis
injury.
Our
offers
an
in-depth
insight
into
driving
immunotoxicity
identifies
potential
strategies
these
mitigate
preserve
immune
function.
Язык: Английский