World Journal of Stem Cells,
Journal Year:
2023,
Volume and Issue:
15(3), P. 52 - 70
Published: March 22, 2023
Ischemic
stroke
(IS)
is
the
most
prevalent
form
of
brain
disease,
characterized
by
high
morbidity,
disability,
and
mortality.
However,
there
still
a
lack
ideal
prevention
treatment
measures
in
clinical
practice.
Notably,
transplantation
therapy
mesenchymal
stem
cells
(MSCs)
has
been
hot
research
topic
stroke.
Nevertheless,
are
risks
associated
with
this
cell
therapy,
including
tumor
formation,
coagulation
dysfunction,
vascular
occlusion.
Also,
growing
number
studies
suggest
that
therapeutic
effect
after
MSCs
mainly
attributed
to
MSC-derived
exosomes
(MSC-Exos).
And
cell-free
mediated
appears
circumvent
many
difficulties
when
compared
it
may
be
promising
new
strategy
for
treating
as
replacement
therapy.
Studies
suppressing
inflammation
via
modulation
immune
response
an
additional
option
IS.
Intriguingly,
MSC-Exos
mediates
inflammatory
following
IS
modulating
central
nervous
system,
peripheral
immunomodulatory
molecules,
thereby
promoting
neurofunctional
recovery
Thus,
paper
reviews
role,
potential
mechanisms,
post-IS
order
identify
targets.
Frontiers in Immunology,
Journal Year:
2023,
Volume and Issue:
13
Published: Feb. 2, 2023
Ischemic
stroke
(IS)
is
one
of
the
most
fatal
diseases.
Neuroimmunity,
inflammation,
and
oxidative
stress
play
important
roles
in
various
complex
mechanisms
IS.
In
particular,
early
proinflammatory
response
resulting
from
overactivation
resident
microglia
infiltration
circulating
monocytes
macrophages
brain
after
cerebral
ischemia
leads
to
secondary
injury.
Microglia
are
innate
immune
cells
that
constantly
monitor
microenvironment
under
normal
conditions.
Once
occurs,
activated
produce
dual
effects
neurotoxicity
neuroprotection,
balance
two
determines
fate
damaged
neurons.
The
activation
defined
as
classical
(M1
type)
or
alternative
(M2
type).
M1
type
secrete
pro-inflammatory
cytokines
neurotoxic
mediators
exacerbate
neuronal
damage,
while
M2
promote
a
repairing
anti-inflammatory
response.
Fine
regulation
M1/M2
microglial
minimize
damage
maximize
protection
has
therapeutic
value.
This
review
focuses
on
interaction
between
other
involved
IS
phenotypic
characteristics,
mechanism
natural
plant
components
regulating
IS,
providing
novel
candidate
drugs
for
drug
development.
International Journal of Molecular Sciences,
Journal Year:
2021,
Volume and Issue:
22(23), P. 13101 - 13101
Published: Dec. 3, 2021
Ischaemic
stroke
involves
the
rapid
onset
of
focal
neurological
dysfunction,
most
commonly
due
to
an
arterial
blockage
in
a
specific
region
brain.
Stroke
is
leading
cause
death
and
common
disability,
with
over
17
million
people
worldwide
suffering
from
each
year.
It
now
well-documented
that
neuroinflammation
immune
mediators
play
key
role
acute
long-term
neuronal
tissue
damage
healing,
not
only
infarct
core
but
also
distal
regions.
Importantly,
these
regions,
termed
sites
secondary
neurodegeneration
(SND),
spikes
may
be
seen
sometime
after
initial
onset,
prior
presence
within
However,
it
acknowledge
that,
despite
mounting
information
describing
following
ischaemic
stroke,
exact
mechanisms
whereby
inflammatory
cells
their
drive
stroke-induced
are
still
fully
understood.
As
result,
current
anti-inflammatory
treatments
have
failed
show
efficacy
clinical
trials.
In
this
review
we
discuss
complexities
post-stroke
neuroinflammation,
specifically
how
affects
outcome
acutely,
chronically,
SND.
We
then
previously
assessed
therapies,
particular
focus
on
anti-inflammatories
repurposed
target
SND-associated
neuroinflammation.
Theranostics,
Journal Year:
2023,
Volume and Issue:
13(15), P. 5561 - 5583
Published: Jan. 1, 2023
Rationale:Recent
studies
indicate
that
microglial
activation
and
the
resulting
inflammatory
response
could
be
potential
targets
of
adjuvant
therapy
for
ischemic
stroke.Many
have
emphasized
a
well-established
function
Annexin-A1
(ANXA1)
in
immune
system,
including
regulation
activation.Nevertheless,
few
therapeutic
interventions
targeting
ANXA1
microglia
stroke
been
conducted.In
present
study,
Tat-NTS,
small
peptide
developed
to
prevent
from
entering
nucleus,
was
utilized.We
discovered
underlying
mechanism
Tat-NTS
protect
against
brain
injury.Methods:
Preclinical
were
performed
using
an
oxygen-glucose
deprivation
reperfusion
(OGD/R)
cell
model
vitro
middle
cerebral
artery
occlusion
(MCAO)
animal
vivo.Confocal
imaging
3D
reconstruction
analyses
detecting
protein
expression
subcellular
localization
vivo.Co-immunoprecipitation
(Co-IP),
immunoblotting,
ELISA,
quantitative
real-time
PCR
(qRT-PCR),
Luciferase
reporter
assay
determining
precise
molecular
mechanism.Measurement
on
cytotoxicity
assessed
by
CCK-8
LDH
assay.TUNEL
staining
used
detect
conditioned
medium-mediated
neuronal
apoptosis.Adeno-associated
viruses
(AAVs)
injected
into
cortex,
striatum
hippocampal
CA1
region
adult
male
Cx3cr1-Cre
mice,
further
verify
neurofunctional
outcome
TTC
staining,
modified
Neurological
Severity
Score
(mNSS)
test,
open
field
test
(OFT),
novel
object
recognition
task
(NORT),
Morris
water
maze
(MWM)
long-term
potentiation
(LTP)
Transmission
electron
microscopy
(TEM).
Results:It
observed
administration
led
shift
nucleus
cytoplasm
injury.Notably,
this
accompanied
increase
SUMOylation
transformation
towards
anti-inflammatory
phenotype.We
confirmed
Tat-NTS-induced
mediated
IKKα
degradation
via
NBR1-dependent
selective
autophagy,
then
blocking
NF-κB
pathway.As
result,
release
pro-inflammatory
factors
IL-1β
TNF-α
reduced
both
vivo
experiments.Furthermore,
we
found
peptide's
protective
effect
relieved
neuron
apoptosis.Finally,
Ivyspring
Acta Cardiologica,
Journal Year:
2024,
Volume and Issue:
79(4), P. 473 - 485
Published: April 20, 2024
Inflammation
plays
a
pivotal
role
in
the
pathogenesis
of
heart
failure
(HF).
This
study
was
aimed
to
potential
association
between
complete
blood
cell
count
(CBC)-derived
inflammatory
biomarkers
and
HF.
Current Opinion in Hematology,
Journal Year:
2021,
Volume and Issue:
28(5), P. 301 - 307
Published: June 28, 2021
Purpose
of
review
In
this
review,
we
will
describe
how
the
combined
ability
platelets
and
neutrophils
to
interact
with
each
other
drives
ischemic
stroke
brain
injury.
Recent
findings
Neutrophils
are
one
first
cells
respond
during
stroke.
Although
animals
models
have
indicated
targeting
improves
outcomes,
clinical
trials
failed
yield
successful
strategies.
Platelets
play
a
critical
role
in
recruiting
sites
injury
by
acting
as
bridge
injured
endothelium.
After
initial
platelet
adhesion,
can
rapidly
bind
through
P-selectin
glycoprotein
Ibα.
addition,
recent
data
implicated
phosphatidylserine
novel
key
regulator
platelet-neutrophil
interactions
setting
Inhibition
procoagulant
decreases
circulating
aggregates
thereby
reduces
infarct
size.
Platelet
binding
alters
neutrophil
function,
which
contributes
associated
This
includes
inducing
release
extracellular
traps,
neurotoxic
pro-thrombotic,
leading
impaired
outcomes.
Summary
Platelet-neutrophil
significantly
contribute
pathophysiology
Better
understanding
mechanisms
behind
their
formation
downstream
consequences
lead
improved
therapies
for
patients.
International Journal of Molecular Sciences,
Journal Year:
2022,
Volume and Issue:
23(5), P. 2550 - 2550
Published: Feb. 25, 2022
Due
to
aging
of
the
world’s
population,
stroke
has
become
increasingly
prevalent,
leading
a
rise
in
socioeconomic
burden.
In
recent
past,
research
and
treatment
have
key
scientific
issues
that
need
urgent
solutions,
with
sharp
focus
on
stem
cell
transplantation,
which
is
known
treat
neurodegenerative
diseases
related
traumatic
brain
injuries,
such
as
stroke.
Indeed,
therapy
brought
hope
many
patients,
both
animal
clinical
trials.
Mesenchymal
cells
(MSCs)
are
most
commonly
utilized
biological
medical
research,
due
their
pluripotency
universality.
MSCs
often
obtained
from
adipose
tissue
bone
marrow,
transplanted
via
intravenous
injection.
Therefore,
this
review
will
discuss
therapeutic
mechanisms
extracellular
vehicles
(EVs)
secreted
by
for
stroke,
attenuating
inflammation
through
immunomodulation,
releasing
trophic
factors
promote
effects,
inducing
angiogenesis,
promoting
neurogenesis,
reducing
infarct
volume,
replacing
damaged
cells.