Histopathological effects of hypervitaminosis-D and the protective role of fetuin-A in renal, hepatic, and cardiac tissues in a murine model
Scientific Reports,
Год журнала:
2025,
Номер
15(1)
Опубликована: Янв. 7, 2025
Hypervitaminosis
D
leads
to
toxic
effects,
including
hypercalcemia,
which
can
cause
severe
damage
various
organs.
Fetuin-A,
a
glycoprotein
with
anti-inflammatory
properties,
may
protect
tissues
from
such
damage.
This
study
explores
the
role
of
Fetuin-A
in
mitigating
hypervitaminosis
D-induced
renal,
hepatic,
and
cardiac
tissues.
The
objectives
this
were
to:
(1)
Assess
extent
tissue
high-dose
vitamin
murine
model
by
examining
histopathological
changes
liver,
kidney
heart.
(2)
Investigate
Fetuin-A's
protective
effect
against
Thirty-six
albino
rats
divided
into
four
groups:
control,
toxicity,
(3)
+
D,
(4)
only.
Vitamin
was
administered
subcutaneously
at
250
μg/20
g/day
for
3
days.
given
100
μl/20
g,
starting
7
days
before
treatment.
Histopathological
analysis
kidney,
heart
performed
using
H&E
Alizarin
Red
staining
findings
analysed
statistically.
toxicity
caused
significant
damage,
apoptosis,
inflammation,
calcification
kidneys,
Pre-treatment
reduced
preserving
architecture.
Fetuin-A-only
showed
no
or
calcification.
provided
statistically
protection
reducing
oxidative
stress
affected
These
suggest
could
be
potential
therapeutic
agent
D.
Язык: Английский
JNK inhibition mitigates sepsis-associated encephalopathy via attenuation of neuroinflammation, oxidative stress and apoptosis
Metabolic Brain Disease,
Год журнала:
2025,
Номер
40(3)
Опубликована: Март 13, 2025
Язык: Английский
JAK/STAT inhibitors mitigate sepsis‐associated cerebral and cognitive injury
Fundamental and Clinical Pharmacology,
Год журнала:
2025,
Номер
39(3)
Опубликована: Апрель 7, 2025
Abstract
Background
Sepsis
is
a
life
threatening
condition
which
triggers
multiple
organ
failure.
Sepsis‐associated
encephalopathy
(SAE)
more
prevalent
form
of
sepsis
involves
acute
and
long‐term
cerebral
impairment.
JAK/STAT
pathway
one
the
most
crucial
signaling
cascades
promote
neuroinflammation.
Objectives
The
present
investigation
was
designed
to
explore
possible
role
inhibitors
in
sepsis‐induced
injury
cognitive
impairment
mice.
Methods
Swiss
Albino
mice
underwent
cecal
ligation
puncture
(CLP)
induce
sepsis‐associated
deficits.
Tofacitinib
baricitinib
were
administered
orally
hour
before
CLP,
followed
by
six
days
post‐CLP
administration.
From
7‐12,
behavioral
changes
assessed
through
various
tests,
including
open
field
(locomotor
activity
non‐associative
memory),
inhibitory
avoidance
(aversive
novel
object
recognition
(recognition
Morris‐Water
maze
tests
(spatial
learning
memory).
Neuronal
(S‐100
calcium‐binding
protein
B,
S100B
neuronal
specific
enolase,
NSE)
inflammation
(TNF‐α)
serum.
Further,
oxidative
mouse
brain
evaluated
measuring
malondialdehyde
reduced
glutathione
levels.
Results
inhibitors,
tofacitinib
(7.5
15
mg/kgper
os)
(5
10
os),
significantly
ameliorated
deficits
non‐associative,
aversive,
spatial
memory
treatment
decreased
TNF‐α,
Malondialdehyde,
S‐100B
NSE
with
while
increasing
levels
glutathione.
Conclusion
neuroinflammation,
stress,
damage
enhancing
function.
Язык: Английский
Bridging systemic metabolic dysfunction and Alzheimer’s disease: the liver interface
Molecular Neurodegeneration,
Год журнала:
2025,
Номер
20(1)
Опубликована: Май 28, 2025
Abstract
Alzheimer’s
disease
(AD)
is
increasingly
recognized
as
a
systemic
disorder
with
substantial
metabolic
component,
where
the
liver
significantly
impacts
brain
via
liver-brain
axis.
Key
mechanisms
include
liver’s
role
in
clearing
peripheral
β-amyloid
(Aβ),
influence
of
hepatic
enzymes
and
metabolites
on
cognitive
decline,
effects
disorders
AD
progression.
Hepatokines,
liver-secreted
proteins
including
fibroblast
growth
factor
(FGF)-21,
selenoprotein
P
(SELENOP),
Fetuin-A,
Midbrain
astrocyte-derived
neurotrophic
(MANF),
apolipoprotein
J
(ApoJ),
sex
hormone-binding
globulin
(SHBG),
Adropin
Angiopoietin-like
protein
3
(ANGPTL3),
could
regulate
insulin
sensitivity,
lipid
metabolism,
oxidative
stress,
immune
responses,
support.
These
pathways
are
closely
linked
to
core
pathologies,
Aβ
aggregation,
tau
hyperphosphorylation,
neuroinflammation,
stress
mitochondrial
dysfunction.
Lifestyle
interventions,
exercise
dietary
modifications,
that
hepatokines
expression
may
offer
novel
preventive
therapeutic
strategies
for
AD.
This
review
synthesizes
current
knowledge
crosstalk
AD,
emphasizing
mechanistic
bridging
dysfunction
neurodegeneration
underscores
diagnostic
potential
addressing
AD’s
complex
pathology.
Язык: Английский
A focus on c-Jun-N-terminal kinase signaling in sepsis-associated multiple organ dysfunction: Mechanisms and therapeutic strategies
International Immunopharmacology,
Год журнала:
2024,
Номер
143, С. 113552 - 113552
Опубликована: Ноя. 15, 2024
Язык: Английский
Polydopamine modification of polydimethylsiloxane for multifunctional biomaterials: Immobilization and stability of albumin and fetuin-A on modified surfaces
Biointerphases,
Год журнала:
2023,
Номер
18(6)
Опубликована: Ноя. 1, 2023
The
surface
of
polydimethylsiloxane
(PDMS)
can
be
modified
to
immobilize
proteins;
however,
most
existing
approaches
are
limited
complex
reactions
and
achieving
multifunctional
modifications
is
challenging.
This
work
applies
a
simple
technique
modify
PDMS
using
polydopamine
(PDA)
investigates
immobilization
multiple
proteins.
surfaces
were
characterized
in
detail
stability
was
assessed,
demonstrating
that
buffer
solution,
PDA
modification
maintained
without
an
effect
on
properties.
Bovine
serum
albumin
(BSA)
bovine
fetuin-A
(Fet-A)
used
as
model
biomolecules
for
simultaneous
or
sequential
understand
their
use
backfilling
functionalization.
Based
125I
radiolabeling,
amounts
BSA
Fet-A
determined
close
double
obtained
control
surfaces.
Following
elution
with
sodium
dodecyl
sulfate,
around
67%
63%
retained
the
surface.
amount
immobilized
protein
influenced
by
process
(simultaneous
sequential)
affinity
With
modification,
balanced
level
both
proteins
could
achieved,
whereas
process,
initially
more
strongly
attached.
After
incubation
plasma
fetal
serum,
PDA-modified
over
90%
immobilized.
demonstrates
biological
environments
also
play
important
role
binding
conjugated
combination
methods
provides
fundamental
knowledge
tailoring
PDMS-based
biomaterials
applications
cell-material
interactions,
biosensing,
medical
devices.
Язык: Английский
Fetuin-A level in patients with untreated thyroid dysfunction
Alaa Salman Idan,
MohdPouzi Hamzah,
Mahmoud Shakir Khudhair
и другие.
The Ukrainian Biochemical Journal,
Год журнала:
2024,
Номер
96(1), С. 60 - 72
Опубликована: Фев. 23, 2024
Fetuin-A,
a
plasma
glycoprotein,
has
been
demonstrated
to
play
an
essential
role
in
the
pathogenesis
of
several
metabolic
disorders.
This
study
aimed
estimate
fetuin-A
serum
level
patients
with
newly
diagnosed
primary
hyperthyroidism
(PHT)
and
subclinical
hypothyroidism
(SCH)
examine
its
correlation
thyroid
hormones
level,
age
sex
patients.
The
involved
90
untreated
dysfunction
verified
function
test
(45
PHT
45
SCH)
control
subjects.
Triiodothyronin
(T3),
tetraiodothyronin
(T4),
stimulating
hormone
(TSH)
concentrations
were
measured
enzyme-linked
fluorescent
assay
(ELFA),
concentration
was
immunosorbent
(ELISA).
It
that
significantly
higher
group
as
compared
showed
significant
positive
T3
level.
In
SCH
group,
lower
negative
TSH
Fetuin-A
rose
unaffected
by
all
studied
groups.
perfect
AUC
value
obtained
for
comparison
between
groups
suggests
potential
use
reliable
diagnostic
marker
differentiate
these
two
conditions.
Язык: Английский
Total Flavonoids of Eucommia ulmoides Oliver Protects Cardiomyocytes against Lipopolysaccharide-Induced Injury by Regulating microRNA-494 Expression
Chen Sun,
Xueli Ren,
Feini Wu
и другие.
Indian Journal of Pharmaceutical Sciences,
Год журнала:
2024,
Номер
86(2)
Опубликована: Янв. 1, 2024
To
explore
the
protective
mechanism
of
total
flavonoids
from
Eucommia
ulmoides
Oliver
leaves
(thin-film
electroluminescent)
on
lipopolysaccharide-induced
cardiomyocyte
H9C2
injury.
Cardiomyocytes
were
divided
into
control,
lipopolysaccharides,
lipopolysaccharides+thin-film
electroluminescent-low
group,
electroluminescent-middle,
electroluminescent-high,
lipopolysaccharides+microRNA-negative
lipopolysaccharides+microRNA-494,
electroluminescent+anti-microRNA-negative
and
electroluminescent+anti-microRNA-494
groups.
The
commercial
kits
used
to
evaluate
superoxide
dismutase
glutathione
peroxidase
activities,
as
well
malondialdehyde
levels.
Flow
cytometry
was
utilized
for
estimation
cell
apoptosis.
Western
blotting
employed
detect
cleaved
caspase-3
caspase-9
protein
Reverse
transcription-quantitative
polymerase
chain
reaction
selected
microRNA-494
expression.
Lipopolysaccharides
significantly
decreased
levels,
increased
induced
apoptosis,
upregulated
levels
in
cardiomyocytes,
suggesting
that
lipopolysaccharides
facilitated
oxidative
stress
Thin-film
electroluminescent
overtly
weakened
apoptosis
a
dose-dependent
mode.
partly
overturned
downregulation
expression
cardiomyocytes.
Furthermore,
elevation
impaired
lipopolysaccharides-induced
In
addition,
knockdown
thin-film
mediated
repressive
effects
could
alleviate
which
achieved
by
upregulating
Язык: Английский
Knockdown of OLFM4 protects cardiomyocytes from sepsis by inhibiting apoptosis and inflammatory responses
Hailu Chen,
Hailu Chen,
Guihua Fang
и другие.
Allergologia et Immunopathologia,
Год журнала:
2024,
Номер
52(5), С. 15 - 20
Опубликована: Сен. 1, 2024
Sepsis
is
a
systemic
inflammatory
response
that
can
result
in
cardiac
insufficiency
or
heart
failure
known
as
septic
myocardial
injury.
A
previous
study
identified
OLFM4
an
important
gene
sepsis
through
bioinformatics
analysis.
However,
there
limited
research
on
the
regulatory
functions
of
sepsis-triggered
injury,
and
related
molecular
mechanisms
remain
unclear.
In
this
study,
protein
expression
was
found
to
be
significantly
elevated
LPS-stimulated
H9C2
cells,
its
suppression
enhanced
cell
proliferation
reduced
apoptosis
LPS-triggered
cells.
The
factors
TNF-α,
IL-6,
IL-1β
were
increased
after
LPS
treatment,
these
effects
mitigated
silencing
OLFM4.
Moreover,
it
confirmed
inhibition
attenuated
NF-κB
signaling
pathway.
conclusion,
knockdown
protected
cardiomyocytes
from
by
inhibiting
responses
via
These
findings
provide
insights
into
progression
Язык: Английский