Cell Biochemistry and Function,
Journal Year:
2024,
Volume and Issue:
42(2)
Published: March 1, 2024
Abstract
Cerebral
ischemic
damage
is
prevalent
and
the
second
highest
cause
of
death
globally
across
patient
populations;
it
as
a
substantial
reason
morbidity
mortality.
Mesenchymal
stromal
cells
(MSCs)
have
garnered
significant
interest
potential
treatment
for
cerebral
damage,
shown
in
stroke,
because
their
potent
intrinsic
features,
which
include
self‐regeneration,
immunomodulation,
multi‐potency.
Additionally,
MSCs
are
easily
obtained,
isolated,
cultured.
Despite
this,
there
number
obstacles
that
hinder
effectiveness
MSC‐based
treatment,
such
adverse
microenvironmental
conditions
both
vivo
vitro.
To
overcome
these
obstacles,
naïve
MSC
has
undergone
modification
processes
to
enhance
its
innate
therapeutic
qualities.
Genetic
preconditioning
(with
medications,
growth
factors,
other
substances)
two
main
categories
into
techniques
can
be
separated.
This
field
advanced
significantly
still
attracting
attention
innovation.
We
examine
cutting‐edge
methods
preserving
even
improving
natural
biological
functions
relation
adhesion,
migration,
homing
target
site,
survival,
delayed
premature
senescence.
address
use
genetically
altered
stroke‐induced
damage.
Future
strategies
result
addressing
difficulties
associated
with
also
discussed.
Antioxidants,
Journal Year:
2022,
Volume and Issue:
11(12), P. 2377 - 2377
Published: Nov. 30, 2022
Cerebral
ischemic
stroke
is
characterized
by
acute
ischemia
in
a
certain
part
of
the
brain,
which
leads
to
brain
cells
necrosis,
apoptosis,
ferroptosis,
pyroptosis,
etc.
At
present,
there
are
limited
effective
clinical
treatments
for
cerebral
stroke,
and
recovery
blood
circulation
will
lead
ischemia-reperfusion
injury
(CIRI).
involves
many
pathological
processes
such
as
oxidative
stress,
inflammation,
mitochondrial
dysfunction.
Nuclear
factor
erythroid
2-related
2
(Nrf2),
one
most
critical
antioxidant
transcription
factors
cells,
can
coordinate
various
cytoprotective
inhibit
stress.
Targeting
Nrf2
considered
potential
strategy
prevent
treat
injury.
During
ischemia,
participates
signaling
pathways
Keap1,
PI3K/AKT,
MAPK,
NF-κB,
HO-1,
then
alleviates
or
CIRI
inhibiting
anti-inflammation,
maintaining
homeostasis,
protecting
blood–brain
barrier,
ferroptosis.
In
this
review,
we
have
discussed
structure
Nrf2,
mechanisms
related
research
on
treatment
through
pathway
recent
years,
expounded
important
role
future
stroke.
International Immunopharmacology,
Journal Year:
2023,
Volume and Issue:
118, P. 110047 - 110047
Published: March 28, 2023
Our
previous
studies
have
shown
that
berberine
can
improve
the
nerve
function
deficits
in
ischemic
stroke
by
inhibiting
inflammation.
The
cellular
communication
between
astrocytes
and
neurons
via
exosomes
might
affect
neurological
after
stroke,
which
plays
a
vital
role
therapy
of
stroke.The
present
study
focused
on
effects
released
from
induced
glucose
oxygen
deprivation
model
with
pretreatment
(BBR-exos)
treatment
for
its
regulatory
mechanism.Oxygen-glucose-deprivation/Reoxygenation
(OGD/R)-treated
primary
cells
were
used
to
mimic
cerebral
ischemia/reperfusion
conditions
vitro.
With
BBR-exos
(OGD/R-exos),
cell
viability
was
detected.
C57BL/6J
mice
establish
middle
artery
occlusion/reperfusion
(MCAO/R)
model.
anti-neuroinflammation
OGD/R-exos
evaluated.
Subsequently,
key
miRNA
identified
exosomal
sequencing
validation.
miR-182-5p
inhibitors
provided
verify
Finally,
binding
sites
Rac1
predicted
online
verified
using
dual-luciferase
reporter
assay.BBR-exos
both
improved
decreased
activity
OGD/R-induced
neurons,
expression
IL-1β,
IL-6
TNF-α
(all
P
＜
0.05),
reduced
neuronal
injury
inhibited
neuroinflammation
Vitro.
And
showed
better
(P
0.05).
same
effect
has
been
vivo
experiments:
MCAO/R
Likewise,
results
highly
expressed
targeting
0.05).BBR-exos
carry
injured
inhibit
Rac1,
could
brain
stroke.
Journal of Neuroinflammation,
Journal Year:
2024,
Volume and Issue:
21(1)
Published: Jan. 29, 2024
Microglia
is
the
major
contributor
of
post-stroke
neuroinflammation
cascade
and
crucial
cellular
target
for
treatment
ischemic
stroke.
Currently,
endogenous
mechanism
underlying
microglial
activation
following
stroke
remains
elusive.
Serglycin
(SRGN)
a
proteoglycan
expressed
in
immune
cells.
Up
to
now,
role
SRGN
on
largely
unexplored.
Abstract
Objectives
FTO
is
known
to
be
involved
in
cerebral
ischemia/reperfusion
(I/R)
injury.
However,
its
related
specific
mechanisms
during
this
condition
warrant
further
investigations.
This
study
aimed
at
exploring
the
impacts
of
and
FYN/DRP1
axis
on
mitochondrial
fission,
oxidative
stress
(OS),
ferroptosis
I/R
injury
underlying
mechanisms.
Methods
The
models
were
established
mice
via
temporary
middle
artery
occlusion/reperfusion
(tMCAO/R)
hypoxia/reoxygenation
induced
mouse
hippocampal
neurons
oxygen–glucose
deprivation/reoxygenation
(OGD/R).
After
gain‐
loss‐of‐function
assays,
gene
expression
was
detected,
along
with
examination
OS‐
ferroptosis‐related
marker
levels,
neuronal
degeneration
infarction,
cell
viability
apoptosis.
binding
FYN,
m6A
modification
levels
interaction
between
FYN
Drp1
evaluated.
Results
downregulated
upregulated
tMCAO/R
OGD/R
models.
overexpression
inhibited
OS,
suppress
mice,
which
reversed
by
overexpressing
FYN.
also
suppressed
fission
increase
survival
inhibit
apoptosis
models,
aggravated
additionally
inhibiting
DRP1.
inactive
signaling,
thus
reducing
enhancing
cells.
Conclusions
through
modification,
thereby
subduing
activity
relieving
Journal of Neuroimmune Pharmacology,
Journal Year:
2025,
Volume and Issue:
20(1)
Published: Feb. 3, 2025
Stroke
represents
a
significant
burden
on
global
health
and
the
economy,
with
high
mortality
rates,
disability,
recurrence.
Ischemic
stroke
is
serious
condition
that
occurs
when
blood
vessel
in
brain
interrupted,
reducing
supply
to
affected
area.
Inflammation
component
pathophysiology.
Neuroinflammation
triggered
following
acute
ischemic
ictus,
where
blood–brain
barrier
(BBB)
breaks
down,
causing
damage
endothelial
cells.
The
will
eventually
generate
oxidative
stress,
activate
pathological
phenotypes
of
astrocytes
microglia,
lead
neuronal
death
neurovascular
unit.
As
result,
unleashes
robust
neuroinflammatory
response,
which
can
further
worsen
neurological
outcomes.
complex
process
involved
repair.
Finding
new
neuroinflammation
molecular
targets
essential
develop
effective
safe
novel
treatment
approaches
against
stroke.
Accumulating
studies
have
investigated
pharmacological
properties
cannabinoids
(CBs)
for
many
years,
recent
research
has
shown
their
potential
therapeutic
use
treating
rodent
models.
These
findings
revealed
promising
impacts
CBs
cellular
ameliorating
deficits.
In
this
review,
we
explore
possibility
administration
mitigating
caused
by
We
summarize
results
from
several
preclinical
evaluating
efficacy
anti-inflammatory
interventions
Although
convincing
evidence
implies
targeting
are
stroke,
translating
these
into
clinical
setting
proven
be
challenging.
translation
hurdle
due
essence
ability
cause
anxiety,
cognitive
deficit,
psychosis.
Future
warranted
address
dose-beneficial
effect
trials
stroke-related
treatment.
