Heliyon,
Год журнала:
2024,
Номер
10(20), С. e39076 - e39076
Опубликована: Окт. 1, 2024
Remote
ischemic
preconditioning
(RIPC)
represents
a
clinically
feasible
method
for
safeguarding
vital
organs
against
injury.
However,
its
specific
role
in
cerebral
ischemia-reperfusion
(I/R)
injury
remains
to
be
definitively
elucidated.
In
this
study,
we
investigated
the
neuroprotective
effects
of
RIPC
on
mice
at
7
days
post-cerebral
I/R
and
involvement
mitophagy
mitochondrial
dysfunction.
Cerebral
led
impaired
brain
function,
as
well
structural
functional
damage
mitochondria.
Notably,
treatment
ameliorated
neurological
dysfunction
induced
by
I/R.
Compared
with
group,
expression
levels
NeuN,
MBP,
PDH,
Tom20
were
significantly
elevated
RIPC+I/R
group.
Furthermore,
mitochondria
group
exhibited
more
intact
structure
compared
those
subjected
injury,
markedly
increased
ATP
content,
ADP
TAN
level
glucose
uptake
while
upregulating
Parkin,
Pink1
P62
proteins;
it
also
reduced
both
volume
foci
number
autophagosomes
along
decreasing
LC3B
II/I
ratio.
conclusion,
may
exert
inhibiting
excessive
during
subacute
stages
following
an
stroke.
Research Square (Research Square),
Год журнала:
2024,
Номер
unknown
Опубликована: Фев. 7, 2024
Abstract
Objectives:
Objective
To
investigate
the
neuroprotective
effect
and
mechanism
of
Rhodiola
rosea
glycosides(SAL)
on
cerebral
ischemia/reperfusion
injury
(CIRI)
rats
through
mitochondrial
autophagy
pathway
mediated
by
estrogen
receptor
β
(ERβ)/B-cell
lymphoma-2/adenovirus
E1B
interacting
protein
3
(BNIP3).
Methods:
135
SD
were
divided
into
OVX
model
groups
(OVX+MCAO/R),estradiol
control
group
(OVX+MCAO/R+E2),
ERβ
inhibitor
(OVX+MCAO/R+SAL+PHTPP),
(OVX+MCAO/R+SAL+Mdivi-1),
SAL
low,medium,
high
dose
(OVX+MCAO/R+SAL).
MCAO/R+SAL),
middle
artery
embolism
(MCAO/R)
was
constructed
using
wire
method,
reperfusion
performed
for
24h
after
1h
ischaemia.
Neurological
function
scoring
reperfusion;
TTC
staining
used
to
detect
volume
infarction;
water
content
brain
tissue
determined
wet
dry
gravimetry;
permeability
blood-brain
barrier
Evans
blue
(EB)
content;
levels
oestrogen
(E2),
superoxide
dismutase
(SOD)
malondialdehyde
(MDA)
analysed
kit;
neuron
pathology
observed
ischemic
side
hematoxylin
eosin
(HE)
staining;
damage
in
Nissl
kit.
observe
neuronal
tissue;
transmission
electron
microscopy
(TEM)
autophagosomes;
Western
blotting
expression
autophagy-related
proteins,
BNIP3,
NIX,
Beclin-1
LC3.
Results:
There
no
statistical
difference
(P>0.05)
Longa
score,
TTC,
content,
EB,
E2
oxidative
stress
level,
HE,
Niehl's
Con
compared
with
group,
indicating
that
removal
ovaries
had
subsequent
experiments;
whereas,
there
a
statistically
significant
(P<0.05)
decrease
proteins
MCAO/R
groups,
Mdivi-1
PHTPP
played
protective
role
against
neural
SAL-H
group.
It
indicated
exerted
nerve
injury;
whereas
two
PHTPP,
significantly
different
reversed
decreased
suggesting
may
protect
cells
ERβ-mediated
autophagy.
Conclusions:
Conclusion
improve
neurological
modulating
level
ERβ/BNIP3-mediated
self,
providing
new
way
drug
development
based
combined
as
ischemia.
International Heart Journal,
Год журнала:
2024,
Номер
65(3), С. 517 - 527
Опубликована: Май 30, 2024
Myocardial
infarction/reperfusion
(I/R)
injury
significantly
impacts
the
health
of
older
individuals.
We
confirmed
that
level
lncRNA
Peg13
was
downregulated
in
I/R
injury.
However,
detailed
function
myocardial
has
not
yet
been
explored.To
detect
Peg13,
vivo
model
constructed.
RT-qPCR
employed
to
investigate
RNA
levels,
and
Western
blotting
performed
assess
levels
endoplasmic
reticulum
stress
apoptosis-associated
proteins.
EdU
staining
cell
proliferation.I/R
therapy
dramatically
produced
injury,
increased
infarct
area,
decreased
amount
tissues
mice.
In
addition,
hypoxia/reoxygenation
(H/R)
notably
induced
apoptosis
promoted
(ER)
HL-1
cells,
while
overexpression
reversed
these
phenomena.
Additionally,
may
increase
Sirt1
through
binding
miR-34a.
Upregulation
H/R-induced
ER
via
regulation
miR-34a/Sirt1
axis.LncRNA
reduces
mediation
axis.
Hence,
our
research
might
shed
new
lights
on
developing
strategies
for
treatment
Heliyon,
Год журнала:
2024,
Номер
10(20), С. e39076 - e39076
Опубликована: Окт. 1, 2024
Remote
ischemic
preconditioning
(RIPC)
represents
a
clinically
feasible
method
for
safeguarding
vital
organs
against
injury.
However,
its
specific
role
in
cerebral
ischemia-reperfusion
(I/R)
injury
remains
to
be
definitively
elucidated.
In
this
study,
we
investigated
the
neuroprotective
effects
of
RIPC
on
mice
at
7
days
post-cerebral
I/R
and
involvement
mitophagy
mitochondrial
dysfunction.
Cerebral
led
impaired
brain
function,
as
well
structural
functional
damage
mitochondria.
Notably,
treatment
ameliorated
neurological
dysfunction
induced
by
I/R.
Compared
with
group,
expression
levels
NeuN,
MBP,
PDH,
Tom20
were
significantly
elevated
RIPC+I/R
group.
Furthermore,
mitochondria
group
exhibited
more
intact
structure
compared
those
subjected
injury,
markedly
increased
ATP
content,
ADP
TAN
level
glucose
uptake
while
upregulating
Parkin,
Pink1
P62
proteins;
it
also
reduced
both
volume
foci
number
autophagosomes
along
decreasing
LC3B
II/I
ratio.
conclusion,
may
exert
inhibiting
excessive
during
subacute
stages
following
an
stroke.
