Research Square (Research Square),
Год журнала:
2023,
Номер
unknown
Опубликована: Дек. 4, 2023
Abstract
Background
The
long-term
feeding
of
high-concentrate
diets
to
ruminants
will
damage
the
structure
and
function
their
rumen
flora,
leading
changes
in
gastrointestinal
patterns
digestive
nutrients
metabolic
factors,
causing
subacute
acidosis
(SARA).
Methods
28
small-tailed
Han
sheep
were
randomly
selected
divided
into
three
groups,
namely
control
group,
SARA
model
treatment
group.
group
was
fed
low
concentrate
fodder,
high
HC
first
then
LC
after
successfully
establishing
(n
=
9).
Results
SARA-model
had
concentrations
lipopolysaccharide
(LPS)
fluid
blood,
whereas
tumor
necrosis
factor-α
(TNF-α)
significantly
elevated
fluid,
with
no
difference
blood.
levels
inflammation-related
proteins,
cyclooxygenase-2
(COX-2),
interleukin-6
(IL-6),
TNF-α,
Toll-like
receptor-4
(TLR-4),
increased
epithelium
sheep.
Phosphorylation
nuclear
transcription
factor-κB
(NF-κB)
mitogen-activated
protein
kinases
(MAPKs)
higher
than
those
groups.
phosphorylation
NF-κB
MAPKs
inflammatory
mediators
factors
abdominal
sac
dorsal
sac.
expression
tight
junction
proteins
ZO-1,
occludin,
claudin-1
claudin-4
decreased
compared
that
light
chain
3
(LC-3)
sheep,
while
trend
autophagy
substrate
sequestosome-1
(P62)
opposite
LC-3.
Conclusions
These
results
indicate
leads
a
concentration
ruminal
LPS,
which
increases
synthesis
pro-inflammatory
cytokines
epithelium,
through
over-activation
MAPK
pathways,
thereby
inducing
rumenitis,
damaging
integrity
epithelium;
moreover,
is
more
serious
In
process
gastritis,
involved
regulation
inhibition
response.
Experimental Gerontology,
Год журнала:
2024,
Номер
192, С. 112451 - 112451
Опубликована: Май 9, 2024
The
NLRP3
inflammasome
is
critically
involved
in
the
development
of
depression.
E3
ubiquitin
ligase
TRIM31
negatively
regulates
this
process
by
promoting
degradation
through
ubiquitin-proteasome
pathway.
Modified
Danzhi
Xiaoyaosan
(MDZXYS)
has
shown
good
therapeutic
effect
both
preclinical
and
clinical
depression
treatments,
yet
underlying
mechanisms
its
antidepressant
effects
are
not
fully
understood.
In
present
study,
we
aimed
to
explore
MDZXYS,
focusing
on
activation
ubiquitin-mediated
degradation.
We
employed
rats
with
induced
chronic
unpredictable
mild
stress
(CUMS)
conducted
various
behavioral
tests,
including
sucrose
preference,
forced
swimming,
open
field
tests.
Neuronal
damage
CUMS-treated
was
assessed
using
Nissl
staining.
measured
proinflammatory
cytokine
levels
ELISA
kits
analyzed
NLRP3/TRIM31
protein
expression
via
Western
blotting
immunofluorescence
Our
results
disclosed
that
MDZXYS
reversed
CUMS-induced
depression-like
behaviors
rats,
reduced
(IL-1β),
ameliorated
neuronal
prefrontal
cortex.
Additionally,
CUMS
activated
cortex
upregulated
TRIM31.
After
administration,
inflammasome-associated
proteins
reduced,
while
level
further
increased.
Through
co-localized
staining,
observed
a
significant
elevation
co-localization
group.
These
findings
suggest
inhibiting
inflammasome-mediated
neuroinflammation
modulating
TRIM31signaling
pathway
may
underlie
support
targeting
as
novel
approach
for
prevention
treatment
Journal of Nanobiotechnology,
Год журнала:
2024,
Номер
22(1)
Опубликована: Авг. 12, 2024
The
secondary
injury
is
more
serious
after
traumatic
brain
(TBI)
compared
with
primary
injury.
Release
of
excessive
reactive
oxygen
species
(ROS)
and
Ca2+
influx
at
the
damaged
site
trigger
Herein,
a
neutrophil-like
cell
membrane-functionalized
nanoparticle
was
developed
to
prevent
ROS-associated
NCM@MP
composed
three
parts:
(1)
Differentiated
membrane
(NCM)
synthesized,
inflammation-responsive
ability
achieve
effective
targeting
increase
retention
time
Mn3O4
nimodipine
(MP)
in
deep
tissue
via
C-X-C
chemokine
receptor
type
4,
integrin
beta
1
macrophage
antigen-1.
(2)
Nimodipine
used
inhibit
influx,
eliminating
ROS
source.
(3)
further
eradicated
existing
ROS.
In
addition,
also
exhibited
desirable
properties
for
T1
enhanced
imaging
low
toxicity
which
may
serve
as
promising
multifunctional
nanoplatforms
precise
therapies.
our
study,
obviously
alleviated
oxidative
stress
response,
reduced
neuroinflammation,
protected
blood–brain
barrier
integrity,
relieved
edema,
promoted
regeneration
neurons,
improved
cognition
TBI
mice.
This
study
provides
management
relieve
spread
damage.
Scientific Reports,
Год журнала:
2025,
Номер
15(1)
Опубликована: Май 15, 2025
Type
2
diabetes
mellitus
(T2DM)
and
Major
depressive
disorder
(MDD)
act
as
risk
factors
for
each
other,
the
comorbidity
of
both
significantly
increases
all-cause
mortality
rate.
Therefore,
studying
diagnosis
treatment
with
depression
(DD)
is
great
significance.
In
this
study,
we
progressively
identified
hub
genes
associated
T2DM
through
WGCNA
analysis,
PPI
networks,
machine
learning,
constructed
ROC
nomogram
to
assess
their
diagnostic
efficacy.
Additionally,
validated
these
using
qRT-PCR
in
hippocampus
DD
model
mice.
The
results
indicate
that
UBTD1,
ANKRD9,
CNN2,
AKT1,
CAPZA2
are
shared
depression,
CNN2
UBTD1
demonstrating
favorable
predictive
model,
(p
>
0.05)
ANKRD9
<
0.01)
were
downregulated,
while
0.001),
AKT1
0.05),
upregulated.
We
have
discussed
mechanisms
action
pathogenesis
therapy
DD,
suggesting
therapeutic
potential,
propose
may
serve
prospective
candidates
DD.
conclusion,
work
offers
new
insights
future
research
on
