Frontiers in Cell and Developmental Biology,
Journal Year:
2021,
Volume and Issue:
9
Published: Dec. 1, 2021
Notoginsenoside
R1
(NGR1),
the
primary
bioactive
compound
found
in
Panax
notoginseng,
is
believed
to
have
antihypertrophic
and
antiapoptotic
properties,
has
long
been
used
prevent
treat
cardiovascular
diseases.
However,
its
potential
role
prevention
of
diabetic
cardiomyopathy
remains
unclear.
The
present
study
aimed
investigate
mechanism
NGR1
action
high
glucose-induced
cell
injury.
H9c2
cardiomyocytes
were
cultured
a
high-glucose
medium
as
an
in-vitro
model,
apoptotic
cells
visualized
using
TUNEL
staining.
Expression
Nrf2
HO-1
was
measured
Western
blotting
or
reverse
transcription-quantitative
PCR
(RT-qPCR).
small
interfering
(si)
RNA
transfected
into
Opti-MEM
containing
Lipofectamine®
RNAiMAX.
protected
from
death,
apoptosis
hypertrophy
induced
by
glucose
concentration.
auricular
natriuretic
peptide
brain
remarkably
reduced
NGR1-treated
H9C2
cells.
blot
analysis
showed
that
concentration
markedly
inhibited
AMPK,
HO-1,
this
could
be
reversed
treatment.
cardioprotective
effect
attenuated
C,
which
reverses
expression
levels,
suggesting
AMPK
upregulates
gene
expression,
protein
synthesis
secretion.
Transfection
with
siRNA
via
HO-1.
These
results
indicated
injury
AMPK/Nrf2
signaling
downstream
target,
pathway.
We
conclude
effects
result
upregulation
cardiomyocytes.
Our
findings
suggest
treatment
might
provide
novel
therapy
for
cardiomyopathy.
Frontiers in Cardiovascular Medicine,
Journal Year:
2022,
Volume and Issue:
9
Published: Oct. 5, 2022
Background
Metabolic
and
energy
disorders
are
considered
central
to
the
etiology
of
diabetic
cardiomyopathy
(DCM).
Sodium-glucose
cotransporter-2
inhibitors
(SGLT2i)
can
effectively
reduce
risk
cardiovascular
death
heart
failure
in
patients
with
DCM.
However,
underlying
mechanism
has
not
been
elucidated.
Methods
We
established
a
DCM
rat
model
followed
by
treatment
empagliflozin
(EMPA)
for
12
weeks.
Echocardiography,
blood
tests,
histopathology,
transmission
electron
microscopy
(TEM)
were
used
evaluate
phenotypic
characteristics
rats.
The
proteomics
metabolomics
myocardium
performed
identify
potential
targets
signaling
pathways
associated
benefit
SGLT2i.
Results
showed
pronounced
characterized
mitochondrial
pleomorphic,
impaired
lipid
metabolism,
myocardial
fibrosis,
diastolic
systolic
functional
impairments
heart.
To
some
extent,
these
changes
ameliorated
after
EMPA.
A
total
43
proteins
34
metabolites
identified
as
rats
treated
KEGG
analysis
that
arachidonic
acid
is
maximum
number
related
may
be
target
EMPA
treatment.
Fatty
(FA)
metabolism
was
enhanced
hearts,
perturbation
biosynthesis
unsaturated
FAs
enabler
Conclusion
SGLT2i
accumulation
damage
metabolomic
proteomic
data
revealed
SGLT2i,
which
provides
valuable
resource
PLoS ONE,
Journal Year:
2023,
Volume and Issue:
18(5), P. e0281496 - e0281496
Published: May 3, 2023
Diabetes
mellitus
(DM)
is
one
of
the
most
researched
metabolic
diseases
worldwide.
It
leads
to
extensive
complications
such
as
cardiovascular
disease,
nephropathy,
retinopathy,
and
peripheral
central
nervous
system
through
an
inability
produce
or
respond
insulin.
Although
oxidative
stress-mediated
mitophagy
has
been
reported
play
important
role
in
pathogenesis
DM,
specific
studies
are
still
lacking
well
remain
highly
controversial.
Here,
we
found
that
Parkin-mediated
pancreatic
β
cells
under
streptozotocin
(STZ)-diabetic
stress
was
induced
by
Polo-like
kinase
3
(Plk3)
inhibited
transcription
factor
Forkhead
Box
O3A
(FOXO3A).
STZ
induces
mitochondrial
recruitment
Parkin
Plk3-mediated
reactive
oxygen
species
(ROS)
generation,
which
causes
cell
damage.
Conversely,
FOXO3A
acts
negative
feedback
prevent
diabetic
inhibiting
Plk3.
Meanwhile,
antioxidants
including
N-acetylcysteine
(NAC)
natural
COA
water
scientifically
block
these
ROS
Through
a
3D
organoid
ex
vivo
model,
confirmed
not
only
inhibitors
but
also
inhibitory
factors
3-MA
deletion
can
compensate
for
growth
insulin
secretion
stress.
These
findings
suggest
Plk3-mtROS-PINK1-Parkin
axis
novel
process
inhibits
β-cell
may
provide
new
alternatives
effective
diabetes
treatment
strategies
future.