Background:
Severe
heat
stroke
is
often
complicated
by
multiple
organ
failure,
including
liver
injury.
Recent
evidence
indicates
that
the
underlying
mechanism
constitutes
sterile
inflammation
triggered
cell
damage,
in
which
hepatocyte
NOD-like
receptor
family
pyrin
domain-containing
3
inflammasome
activation
and
pyroptosis
play
key
roles.
As
extracellular
histones
act
as
damage-associated
molecular
patterns
mediate
tissue
toxicity
inflammation,
we
aimed
to
investigate
whether
contribute
inducing
following
stroke,
promoting
development
of
injury,
elucidate
potential
mechanisms.
Methods:
Exogenous
were
administered
AML-12
murine
hepatocytes
or
male
aged
8~12
week
mice
hyperthermic
treatment
(at
39°C
a
chamber
with
60%
relative
humidity).
Prior
exposure,
endogenous
neutralized
using
neutralizing
antibodies,
inflammasomes
inhibited
RNA
silencing,
Toll-like
9
was
modulated
pharmacological
agonist
antagonist.
Inflammasome
assembly,
caspase-1
activation,
histological
changes,
enzyme
levels
measured.
Statistical
comparison
more
than
two
groups
performed
one-way
ANOVA
Tukey’s
post-hoc
testing.
The
correlations
analyzed
Pearson’s
correlation
test.
All
experiments
repeated
thrice.
A
p-value
<
0.05
considered
significant.
Results:
Heat
induced
histone
release
into
space
at
correlating
Moreover,
augmented
stroke-induced
injury
both
vitro
vivo
dose-
time-dependent
manner,
whereas
conferred
protection
stroke.
Histones
mediated
through
signaling
pathway,
resulted
inflammation.
Conclusions:
Our
findings
show
are
critical
mediators
aggravate
setting.
Therefore,
suggest
therapeutic
targets
limit
death
Renal Failure,
Journal Year:
2024,
Volume and Issue:
46(1)
Published: May 27, 2024
Acute
kidney
injury
(AKI)
is
one
of
the
most
common
and
severe
clinical
syndromes
diffuse
proliferative
lupus
nephritis
(DPLN),
which
poor
prognosis
indicated
by
aggravated
renal
function
deterioration.
However,
specific
therapy
mechanisms
AKI
in
DPLN
remain
to
be
explored.
Animals,
Journal Year:
2023,
Volume and Issue:
13(14), P. 2343 - 2343
Published: July 18, 2023
In
the
present
study,
fecal
proteomes
of
clinically
healthy
dogs
(HD
=
n.
10),
showing
clinical,
ultrasonographic,
and/or
laboratory
evidence
different
hepatobiliary
dysfunction
(DHD
and
suffering
from
chronic
hepatitis
(CHD
10)
were
investigated
with
an
Ultimate
3000
nanoUPLC
system,
coupled
to
Orbitrap
Fusion
Lumos
Tribrid
mass
spectrometer.
Fifty-two
proteins
canine
origin
identified
qualitatively
in
three
study
groups,
quantitative
differences
found
55
when
comparing
groups.
Quantitatively,
a
total
41
36
differentially
abundant
DHD
CHD
groups
compared
control
HD,
38
resulted
dysregulated
group
as
group.
Among
various
proteins,
differently
fibronectin
haptoglobin
more
feces
than
ones,
leading
us
hypothesize
its
possible
diagnostic/monitoring
role
hepatitis.
On
other
hand,
trefoil
factor
2
was
increased
dogs.
Our
results
show
that
analysis
proteome
is
very
promising
field
case
disorders,
it
able
highlight
both
qualitative
among
included.
Results
need
be
confirmed
western
blotting
further
studies.
Background:
Severe
heat
stroke
is
often
complicated
by
multiple
organ
failure,
including
liver
injury.
Recent
evidence
indicates
that
the
underlying
mechanism
constitutes
sterile
inflammation
triggered
cell
damage,
in
which
hepatocyte
NOD-like
receptor
family
pyrin
domain-containing
3
inflammasome
activation
and
pyroptosis
play
key
roles.
As
extracellular
histones
act
as
damage-associated
molecular
patterns
mediate
tissue
toxicity
inflammation,
we
aimed
to
investigate
whether
contribute
inducing
following
stroke,
promoting
development
of
injury,
elucidate
potential
mechanisms.
Methods:
Exogenous
were
administered
AML-12
murine
hepatocytes
or
male
aged
8~12
week
mice
hyperthermic
treatment
(at
39°C
a
chamber
with
60%
relative
humidity).
Prior
exposure,
endogenous
neutralized
using
neutralizing
antibodies,
inflammasomes
inhibited
RNA
silencing,
Toll-like
9
was
modulated
pharmacological
agonist
antagonist.
Inflammasome
assembly,
caspase-1
activation,
histological
changes,
enzyme
levels
measured.
Statistical
comparison
more
than
two
groups
performed
one-way
ANOVA
Tukey’s
post-hoc
testing.
The
correlations
analyzed
Pearson’s
correlation
test.
All
experiments
repeated
thrice.
A
p-value
<
0.05
considered
significant.
Results:
Heat
induced
histone
release
into
space
at
correlating
Moreover,
augmented
stroke-induced
injury
both
vitro
vivo
dose-
time-dependent
manner,
whereas
conferred
protection
stroke.
Histones
mediated
through
signaling
pathway,
resulted
inflammation.
Conclusions:
Our
findings
show
are
critical
mediators
aggravate
setting.
Therefore,
suggest
therapeutic
targets
limit
death