Biomedicine & Pharmacotherapy,
Journal Year:
2023,
Volume and Issue:
159, P. 114229 - 114229
Published: Jan. 16, 2023
Neurological
disorders
are
characterized
by
high
morbidity,
disability,
and
mortality
rates,
which
seriously
threaten
human
health.
However,
clinically
satisfactory
agents
for
treatment
still
currently
lacking.
Therefore,
finding
neuroprotective
with
minimum
side
effects
better
efficacy
is
a
challenge.
Chinese
herbal
medicine,
particularly
natural
preparations
extracted
from
herbs
or
plants,
has
become
an
unparalleled
resource
discovering
new
agent
candidates.
Astragali
Radix
important
Qi
tonic
drug
in
traditional
medicine
long
medicinal
history.
As
it
good
prevention
effect
on
neurological
disorders.
Here,
the
role
mechanism
of
astragaloside
IV
were
evaluated
discussed
through
previous
research
results.
Related
information
major
scientific
databases,
such
as
PubMed,
MEDLINE,
Web
Science,
ScienceDirect,
Embase,
BIOSIS
Previews,
Cochrane
Central
Register
Controlled
Trials
Library,
covering
between
2001
2021
was
compiled,
using
"Astragaloside
IV"
"Neurological
disorders,"
IV,"
"Neurodegenerative
diseases"
reference
terms.
By
summarizing
results,
we
found
that
may
play
various
mechanisms:
anti-inflammatory,
anti-oxidative,
anti-apoptotic
protection
nerve
cells
regulation
growth
factor,
well
inhibiting
neurodegeneration
promoting
regeneration.
Astragaloside
promising
agent.
determining
its
pharmacological
mechanism,
be
candidate
Medicinal Research Reviews,
Journal Year:
2023,
Volume and Issue:
43(3), P. 614 - 682
Published: Jan. 19, 2023
Abstract
Ferroptosis
is
an
iron‐dependent
cell
death
program
that
characterized
by
excessive
lipid
peroxidation.
Triggering
ferroptosis
has
been
proposed
as
a
promising
strategy
to
fight
cancer
and
overcome
drug
resistance
in
antitumor
therapy.
Understanding
the
molecular
interactions
structural
features
of
ferroptosis‐inducing
compounds
might
therefore
open
door
efficient
pharmacological
strategies
against
aggressive,
metastatic,
therapy‐resistant
cancer.
We
here
summarize
mechanisms
requirements
small
molecules
target
central
players
ferroptosis.
Focus
placed
on
(i)
glutathione
peroxidase
(GPX)
4,
only
GPX
isoenzyme
detoxifies
complex
membrane‐bound
hydroperoxides,
(ii)
cystine/glutamate
antiporter
system
X
c
−
for
regeneration,
(iii)
redox‐protective
transcription
factor
nuclear
erythroid
2‐related
(NRF2),
(iv)
GPX4
repression
combination
with
induced
heme
degradation
via
oxygenase‐1.
deduce
common
ferroptotic
activity
highlight
challenges
development.
Moreover,
we
critically
discuss
potential
natural
products
lead
structures
provide
comprehensive
overview
structurally
diverse
biogenic
bioinspired
trigger
iron
oxidation,
inhibition
thioredoxin/thioredoxin
reductase
or
less
defined
modes
action.
Acta Pharmaceutica Sinica B,
Journal Year:
2023,
Volume and Issue:
13(12), P. 5107 - 5120
Published: June 20, 2023
Oxidative
stress
injury
and
mitochondrial
dysfunction
are
major
obstacles
to
neurological
functional
recovery
after
ischemic
stroke.
The
development
of
new
approaches
simultaneously
diminish
oxidative
resist
is
urgently
needed.
Inspired
by
the
overproduced
reactive
oxygen
species
(ROS)
at
neuron
mitochondria,
multifunctional
nanoparticles
with
ROS-responsiveness
mitochondrial-targeted
(SPNPs)
were
engineered,
achieving
specific
targeting
delivery
controllable
drug
release
penumbra.
Due
nose-to-brain
pathway,
SPNPs
which
encapsulated
in
a
thermo-sensitive
gel
intranasal
administration
directly
delivered
penumbra
bypassing
blood‒brain
barrier
(BBB)
enhancing
efficiency.
potential
for
stroke
treatment
was
systematically
evaluated
Biomolecules,
Journal Year:
2024,
Volume and Issue:
14(3), P. 305 - 305
Published: March 4, 2024
The
majority
of
approved
therapies
for
many
diseases
are
developed
to
target
their
underlying
pathophysiology.
Understanding
disease
pathophysiology
has
thus
proven
vital
the
successful
development
clinically
useful
medications.
Stroke
is
generally
accepted
as
leading
cause
adult
disability
globally
and
ischemic
stroke
accounts
most
common
form
two
main
types.
Despite
its
health
socioeconomic
burden,
there
still
minimal
availability
effective
pharmacological
treatment.
In
this
review,
we
take
an
in-depth
look
at
etiology
stroke,
including
molecular
cellular
changes.
This
followed
by
a
highlight
drugs,
therapies,
complementary
medicines
that
or
undergoing
clinical
trials
treatment
management
stroke.
We
also
identify
unexplored
potential
targets
in
pathogenesis
can
be
exploited
increase
pool
anti-stroke
neuroprotective
agents
through
de
novo
drug
repurposing.
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
14
Published: Jan. 11, 2024
Ischemic
stroke
(IS),
which
is
the
third
foremost
cause
of
disability
and
death
worldwide,
has
inflammation
cell
as
its
main
pathological
features.
IS
can
lead
to
neuronal
release
factors
such
damage-related
molecular
patterns,
stimulating
immune
system
inflammatory
mediators,
thereby
resulting
in
exacerbating
brain
damage.
Currently,
there
are
a
limited
number
treatment
methods
for
IS,
fact
necessitating
discovery
new
targets.
For
this
review,
current
research
on
ischemic
was
summarized.
The
complex
roles
pathways
principal
cells
(microglia,
astrocyte,
neutrophils,
T
lymphocytes,
monocytes/macrophage)
after
discussed.
mechanisms
interactions
cytokines
involved
these
Moreover,
(pyroptosis,
apoptosis,
necroptosis,
PANoptosis,
ferroptosis)
explored.
Finally,
summary
provided
mechanism
action
natural
pharmacological
active
ingredients
IS.
Despite
significant
recent
progress
remain
many
challenges
that
need
be
overcome.
Scientific Reports,
Journal Year:
2024,
Volume and Issue:
14(1)
Published: March 4, 2024
Abstract
Arterial
occlusion-induced
ischemic
stroke
(IS)
is
a
highly
frequent
subtype.
Nuclear
factor
erythroid
2-related
2
(NRF2)
transcription
that
modulates
antioxidant
genes.
Its
role
in
IS
still
unelucidated.
The
current
study
focused
on
constructing
transient
middle
cerebral
artery
occlusion
(tMCAO)
model
for
investigating
the
NRF2-related
mechanism
underlying
ischemia/reperfusion
(I/R)
injury.
Each
male
C57BL/6
mouse
was
injected
with/with
no
specific
NRF2
activator
post-tMCAO.
Changes
blood–brain
barrier
(BBB)-associated
molecule
levels
were
analyzed
using
western-blotting,
PCR,
immunohistochemistry,
and
immunofluorescence
analysis.
within
I/R
decreased
at
24-h
post-ischemia.
activation
improved
brain
edema,
infarct
volume,
neurological
deficits
after
MCAO/R.
Similarly,
sulforaphane
(SFN)
prevented
down-regulated
tight
junction
proteins
occludin
zonula
occludens
1
(ZO-1)
reduced
up-regulated
aquaporin
4
(AQP4)
matrix
metalloproteinase
9
(MMP9)
tMCAO.
Collectively,
exerted
critical
effect
preserving
BBB
integrity
modulating
ferroptosis
inflammation.
Because
related
to
injury
regulation
following
I/R,
this
provides
potential
therapeutic
target
throws
light
clinically
treating
IS.
Frontiers in Molecular Neuroscience,
Journal Year:
2022,
Volume and Issue:
15
Published: May 6, 2022
Millions
of
patients
are
suffering
from
ischemic
stroke,
it
is
urgent
to
figure
out
the
pathogenesis
cerebral
ischemia-reperfusion
(I/R)
injury
in
order
find
an
effective
cure.
After
I/R
injury,
pro-inflammatory
cytokines
especially
interleukin-1β
(IL-1β)
upregulates
brain
cells,
such
as
microglia
and
neuron.
To
ameliorate
inflammation
after
nucleotide-binding
oligomerization
domain
(NOD),
leucine-rich
repeat
(LRR),
pyrin
domain-containing
protein
3
(NLRP3)
inflammasome
well-investigated.
NLRP3
inflammasomes
complicated
complexes
that
activated
by
endogenous
exogenous
danger
signals
participate
inflammatory
response.
The
assembly
activation
lead
caspase-1-dependent
release
cytokines,
interleukin
(IL)-1β
IL-18.
Furthermore,
pyroptosis
a
cell
death
occurs
dependent
manner
on
injury.
In
this
review,
we
summarized
inflammasome;
moreover,
also
concluded
pivotal
role
inhibitors,
targeting
