Molecular Medicine Reports,
Год журнала:
2018,
Номер
unknown
Опубликована: Март 19, 2018
Myocardial
hypertrophy
is
often
associated
with
myocardial
infarction.
Luteolin-7-O-glucoside
(LUTG)
has
the
prosperity
of
preventing
cardiomyocyte
injury.
The
current
study
aimed
to
explore
potential
protective
effect
LUTG
and
its
relevant
mechanisms
in
heart.
To
establish
cardiac
model
vitro,
Angiotensin
II
(Ang
II)
was
used
stimuli
H9c2
cells
this
study.
CCK‑8
assay
showed
that
pretreatment
improved
cell
viability
cardiomyocytes
co‑treated
Ang
ischemia/reperfusion.
decreased
reactive
oxygen
species
levels.
Furthermore,
it
demonstrated
could
reduce
release
amount
lactate
dehydrogenase
recover
catalase
activity
according
flow
cytometry
analysis,
detection,
respectively
II‑H/R‑treated
cells.
In
addition,
analysis
mitigated
apoptosis
induced
by
hypoxia/reoxygenation
model.
Meanwhile,
reverse
transcription‑quantitative
polymerase
chain
reaction
western
blot
assays
apoptosis‑related
genes,
including
poly
(ADP‑ribose)
polymerase,
Fas,
Fasl
Caspase‑3
were
downregulated
at
transcriptional
translational
Notably,
protien
expression
phosphorylated
(p)‑extracellular
signal‑regulated
kinas
(ERK)
1/2,
p‑janus
kinase
p‑P38
reduced,
while
p‑ERK5
elevated
groups
compared
treatment
group.
Based
on
these
results,
suggested
anti‑apoptosis
may
be
regulating
activation
mitogen‑activated
protein
kinases
signaling
pathways.
Cells,
Год журнала:
2022,
Номер
11(19), С. 3049 - 3049
Опубликована: Сен. 29, 2022
Arrhythmogenic
cardiomyopathy
(ACM)
is
an
inherited
disorder
characterized
by
fibro-fatty
infiltration
with
increased
propensity
for
ventricular
arrhythmias
and
sudden
death.
Genetic
variants
in
desmosomal
genes
are
associated
ACM.
Incomplete
penetrance
a
common
feature
ACM
families,
complicating
the
understanding
of
how
external
stressors
contribute
towards
disease
development.
To
analyze
dual
role
genetics
on
progression,
we
developed
one
first
mouse
models
that
recapitulates
human
variant
introducing
murine
equivalent
R451G
into
endogenous
desmoplakin
(DspR451G/+).
Mice
homozygous
this
displayed
embryonic
lethality.
While
DspR451G/+
mice
were
viable
reduced
expression
DSP,
no
presentable
arrhythmogenic
or
structural
phenotypes
identified
at
baseline.
However,
afterload
resulted
cardiac
performance,
chamber
dilation,
accelerated
progression
to
heart
failure.
In
addition,
following
catecholaminergic
challenge,
frequent
prolonged
arrhythmic
events.
Finally,
aberrant
localization
connexin-43
was
noted
baseline,
becoming
more
apparent
stress
via
pressure
overload.
summary,
cardiovascular
key
trigger
unmasking
both
electrical
humanized
models.
Experimental and Therapeutic Medicine,
Год журнала:
2019,
Номер
unknown
Опубликована: Июль 5, 2019
Osteoporosis
is
a
disease
with
worldwide
prevalence
that
involves
severe
loss
of
bone
mineral
density
and
decreased
microarchitecture,
which
increases
the
risk
fracture.
The
present
study
evaluated
effects
isopsoralen
on
osteoblastic
OB‑6
cells
following
hydrogen
peroxide
(H2O2)‑induced
damage
investigated
molecular
mechanisms
involved
in
this
process.
For
vitro
experiments,
osteoblasts
were
treated
H2O2
or
+
then
cell
viability,
apoptosis,
reactive
oxygen
species
(ROS)
production
calcium
accumulation
determined.
Results
demonstrated
treatment
reduced
runt‑related
transcription
factor
2
(RUNX2)
osteocalcin
(OCN)
expression
levels,
deposition,
whilst
markedly
increasing
apoptosis
ROS
production.
However,
(1
µM)
provided
significant
protection
against
H2O2‑induced
alterations
osteoblasts.
In
addition,
effectively
upregulated
protein
tankyrase
β‑catenin
are
main
transductors
Wnt/β‑catenin
pathway.
Of
note,
protective
attenuated
inhibitor
XAV‑939.
conclusion,
findings
evidence
oxidative
stress‑induced
injury
via
signaling
Molecular Medicine Reports,
Год журнала:
2018,
Номер
unknown
Опубликована: Март 19, 2018
Myocardial
hypertrophy
is
often
associated
with
myocardial
infarction.
Luteolin-7-O-glucoside
(LUTG)
has
the
prosperity
of
preventing
cardiomyocyte
injury.
The
current
study
aimed
to
explore
potential
protective
effect
LUTG
and
its
relevant
mechanisms
in
heart.
To
establish
cardiac
model
vitro,
Angiotensin
II
(Ang
II)
was
used
stimuli
H9c2
cells
this
study.
CCK‑8
assay
showed
that
pretreatment
improved
cell
viability
cardiomyocytes
co‑treated
Ang
ischemia/reperfusion.
decreased
reactive
oxygen
species
levels.
Furthermore,
it
demonstrated
could
reduce
release
amount
lactate
dehydrogenase
recover
catalase
activity
according
flow
cytometry
analysis,
detection,
respectively
II‑H/R‑treated
cells.
In
addition,
analysis
mitigated
apoptosis
induced
by
hypoxia/reoxygenation
model.
Meanwhile,
reverse
transcription‑quantitative
polymerase
chain
reaction
western
blot
assays
apoptosis‑related
genes,
including
poly
(ADP‑ribose)
polymerase,
Fas,
Fasl
Caspase‑3
were
downregulated
at
transcriptional
translational
Notably,
protien
expression
phosphorylated
(p)‑extracellular
signal‑regulated
kinas
(ERK)
1/2,
p‑janus
kinase
p‑P38
reduced,
while
p‑ERK5
elevated
groups
compared
treatment
group.
Based
on
these
results,
suggested
anti‑apoptosis
may
be
regulating
activation
mitogen‑activated
protein
kinases
signaling
pathways.
