Acta Physiologica,
Год журнала:
2024,
Номер
240(3)
Опубликована: Янв. 17, 2024
Abstract
Myocardial
infarction
(MI)
and
its
associated
complications
including
ventricular
arrhythmias
heart
failure
are
responsible
for
a
significant
incidence
of
morbidity
mortality
worldwide.
The
ensuing
cardiomyocyte
loss
results
in
neurohormone‐driven
cardiac
remodeling,
which
leads
to
chronic
MI
survivors.
Ivabradine
is
rate
modulation
agent
currently
used
treatment
with
reduced
ejection
fraction.
canonical
target
ivabradine
the
hyperpolarization‐activated
cyclic
nucleotide‐gated
channels
(HCN)
pacemaker
cells.
However,
post‐MI
hearts,
HCN
can
also
be
expressed
ectopically
non‐pacemaker
cardiomyocytes.
There
an
accumulation
intriguing
evidence
suggest
that
possesses
cardioprotective
effects
independent
reduction.
This
review
aims
summarize
discuss
reported
mechanisms
beyond
myocardial
through
various
molecular
prevention
reactive
oxygen
species‐induced
mitochondrial
damage,
improvement
autophagy
system,
intracellular
calcium
cycling,
modification
electrophysiology,
regulation
matrix
metalloproteinases.
The American Journal of Chinese Medicine,
Год журнала:
2025,
Номер
unknown, С. 1 - 25
Опубликована: Март 18, 2025
Myocardial
infarction
(MI)
is
a
significant
threat
to
human
health
worldwide.
Following
MI,
cardiomyocytes
(CMs)
undergo
pyroptosis,
exacerbating
the
damage
caused
by
infarction.
Ginseng
may
play
role
in
alleviating
CM
pyroptosis.
However,
further
exploration
needed
regarding
its
main
active
ingredients
and
effects.
By
employing
network
pharmacology
on
of
ginseng,
MI
molecular
docking
between
such
pyroptosis-related
proteins,
we
screened
for
ingredient
ginseng.
Through
docking,
identified
ginsenoside
Rh2,
which
acts
cell
as
most
likely
that
stably
binds
proteins.
We
subsequently
constructed
neonatal
rat
oxygen–glucose
deprivation
(OGD)
model
vitro
an
mouse
vivo.
Ginsenoside
Rh2
was
administered,
with
losartan
used
positive
control.
In
OGD
model,
increased
viability
primary
CMs
mitigated
OGD-induced
vivo
reduced
decreased
infarct
size,
improved
cardiac
function.
Our
study
provides
novel
therapeutic
strategy
attenuating
The American Journal of Chinese Medicine,
Год журнала:
2025,
Номер
unknown, С. 1 - 16
Опубликована: Март 20, 2025
Oxidative
stress
and
pyroptosis
have
been
established
as
key
contributors
to
myocardial
ischemia-reperfusion
injury
(MIRI).
While
previous
studies
reported
that
electroacupuncture
(EA)
preconditioning
exerted
cardioprotective
effects,
the
underlying
mechanisms
remain
elusive.
Thus,
this
study
aimed
investigate
effects
of
EA
on
oxidative
in
MIRI
rats,
explore
role
nuclear
factor
E2-associated
2
(Nrf2)
throughout
process.
A
model
was
constructed
by
ligating
left
anterior
descending
coronary
artery
for
30
min,
followed
4
h
reperfusion
rats.
Prior
modeling,
rats
were
subjected
at
Neiguan
Point
three
days.
Furthermore,
ML385,
a
Nrf2
inhibitor,
administered
order
examine
regulating
following
preconditioning.
The
results
revealed
improved
ventricular
function
after
reduced
both
infarction
area
cTnT
levels.
Meanwhile,
alleviated
MIRI-induced
pyroptosis,
evidenced
downregulation
ROS,
MDA,
NF-[Formula:
see
text]B
p65,
caspase-1,
IL-1[Formula:
text],
GSDMD-N,
upregulation
SOD
HO-1.
Mechanistically,
up-regulated
enhanced
expression
Nrf2.
However,
its
ability
attenuate
suppressed
inhibition
Taken
together,
our
indicated
attenuated
mitigating
with
playing
vital
protective
mechanism.
Pharmacognosy Magazine,
Год журнала:
2025,
Номер
unknown
Опубликована: Март 25, 2025
Background
Myocardial
ischemia-reperfusion
(MI/R)
injury
is
a
leading
cause
of
myocardial
damage,
characterized
by
apoptosis
and
impaired
cardiac
function.
Dezocine,
mixed
opioid
receptor
agonist/antagonist,
has
shown
potential
in
mitigating
MI/R
injury,
but
its
underlying
mechanisms
remain
unclear.
Purpose
This
study
aimed
to
evaluate
the
effects
dezocine
on
cell
rats
with
focusing
TLR4/NF-κB
signaling
pathway.
Materials
Methods
Thirty-six
Sprague-Dawley
were
randomly
divided
into
three
groups:
sham,
model,
(
n
=
12
each).
The
sham
group
underwent
thoracotomy
without
injury.
model
received
normal
saline
prior
induction,
while
was
administered
dezocine.
Toll-like
4
(TLR4)
nuclear
factor
kappa
B
(NF-κB)
p65
expression
analyzed
using
immunohistochemistry.
Western
blotting
quantified
Bax
Caspase-3
protein
levels
quantitative
polymerase
chain
reaction
assessed
their
mRNA
expression.
Cell
evaluated
via
terminal
deoxynucleotidyl
transferase
dUTP
nick
end
labeling
(TUNEL)
assay.
Results
TLR4
NF-κB
significantly
elevated
groups
compared
notably
lower
versus
group.
followed
similar
trend.
TUNEL
assay
results
demonstrated
higher
rates
group,
showing
marked
reduction
p
<
0.05).
Conclusion
Dezocine
suppresses
pathway,
reducing
suggesting
as
therapeutic
agent
damage.
Acta Physiologica,
Год журнала:
2024,
Номер
240(3)
Опубликована: Янв. 17, 2024
Abstract
Myocardial
infarction
(MI)
and
its
associated
complications
including
ventricular
arrhythmias
heart
failure
are
responsible
for
a
significant
incidence
of
morbidity
mortality
worldwide.
The
ensuing
cardiomyocyte
loss
results
in
neurohormone‐driven
cardiac
remodeling,
which
leads
to
chronic
MI
survivors.
Ivabradine
is
rate
modulation
agent
currently
used
treatment
with
reduced
ejection
fraction.
canonical
target
ivabradine
the
hyperpolarization‐activated
cyclic
nucleotide‐gated
channels
(HCN)
pacemaker
cells.
However,
post‐MI
hearts,
HCN
can
also
be
expressed
ectopically
non‐pacemaker
cardiomyocytes.
There
an
accumulation
intriguing
evidence
suggest
that
possesses
cardioprotective
effects
independent
reduction.
This
review
aims
summarize
discuss
reported
mechanisms
beyond
myocardial
through
various
molecular
prevention
reactive
oxygen
species‐induced
mitochondrial
damage,
improvement
autophagy
system,
intracellular
calcium
cycling,
modification
electrophysiology,
regulation
matrix
metalloproteinases.
