Immunity Inflammation and Disease,
Год журнала:
2024,
Номер
12(4)
Опубликована: Апрель 1, 2024
Abstract
Background
Spinal
cord
injury
(SCI)
is
a
traumatic
neurological
disorder
with
limited
therapeutic
options.
Tumor
protein
p53‐inducible
nuclear
2
(TP53INP2)
involved
in
the
occurrence
and
development
of
various
diseases,
it
may
play
role
during
SCI
via
affecting
inflammation
neuronal
apoptosis.
This
study
investigated
associated
roles
mechanisms
TP53INP2
SCI.
Methods
Mouse
lipopolysaccharide
(LPS)‐induced
BV‐2
cell
models
were
constructed
to
explore
mechanisms.
Histopathological
evaluation
spinal
tissue
was
detected
by
hematoxylin
eosin
staining.
The
Basso,
Beattie,
Bresnahan
score
used
measure
motor
function
mice,
while
water
content
assess
edema.
expression
measured
using
RT‐qPCR.
In
addition,
inflammatory
factors
mice
LPS‐treated
cells
enzyme‐linked
immunosorbent
assay.
Apoptosis
related
levels
flow
cytometry
western
blot
analysis,
respectively.
Results
increased
cells.
results
vivo
vitro
experiments
showed
that
knockdown
inhibited
response
apoptosis
mouse
or
LPS‐induced
Conclusions
After
injury,
upregulated,
CNS Neuroscience & Therapeutics,
Год журнала:
2023,
Номер
29(4), С. 1094 - 1108
Опубликована: Янв. 10, 2023
Abstract
Background
A
growing
body
of
research
shows
that
drug
monomers
from
traditional
Chinese
herbal
medicines
have
antineuroinflammatory
and
neuroprotective
effects
can
significantly
improve
the
recovery
motor
function
after
spinal
cord
injury
(SCI).
Here,
we
explore
role
molecular
mechanisms
Alpinetin
on
activating
microglia‐mediated
neuroinflammation
neuronal
apoptosis
SCI.
Methods
Stimulation
microglia
with
lipopolysaccharide
(LPS)
to
simulate
models
in
vitro,
effect
release
pro‐inflammatory
mediators
LPS‐induced
its
mechanism
were
detected.
In
addition,
a
co‐culture
system
cells
was
constructed
assess
apoptosis.
Finally,
rat
used
study
inflammation,
apoptosis,
axonal
regeneration,
Alpinetin.
Results
inhibits
activity
JAK2/STAT3
pathway.
also
reverse
activated
reactive
oxygen
species
(ROS)
production
decrease
mitochondrial
membrane
potential
(MMP)
PC12
cells.
vivo
inflammatory
response
improves
function.
Conclusion
be
treat
neurodegenerative
diseases
is
novel
candidate
for
treatment
neuroinflammation.
Journal of Translational Medicine,
Год журнала:
2024,
Номер
22(1)
Опубликована: Март 25, 2024
Abstract
Background
The
treatment
of
spinal
cord
injury
(SCI)
has
always
been
a
significant
research
focus
clinical
neuroscience,
with
inhibition
microglia-mediated
neuro-inflammation
as
well
oxidative
stress
key
to
successful
SCI
patient
treatment.
Caffeic
acid
phenethyl
ester
(CAPE),
compound
extracted
from
propolis,
both
anti-inflammatory
and
anti-oxidative
effects,
but
its
therapeutic
effects
have
rarely
reported.
Methods
We
constructed
mouse
contusion
model
administered
CAPE
intraperitoneally
for
7
consecutive
days
after
injury,
methylprednisolone
(MP)
was
used
positive
control.
Hematoxylin–eosin,
Nissl,
Luxol
Fast
Blue
staining
were
assess
the
effect
on
structures
nervous
tissue
SCI.
Basso
Mouse
Scale
scores
footprint
analysis
explore
recovery
motor
function
by
mice.
Western
blot
immunofluorescence
assessed
levels
inflammatory
mediators
stress-related
proteins
in
vivo
vitro
Further,
reactive
oxygen
species
(ROS)
within
cytoplasm
detected
using
an
ROS
kit.
Changes
mitochondrial
membrane
potential
5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethyl-imidacarbocyanine
iodide.
Mechanistically,
western
examine
SIRT1/PGC1α/DRP1
signaling
pathway.
Results
CAPE-treated
mice
showed
less
neuronal
loss,
more
survival,
reduced
demyelination.
Interestingly,
treated
better
function.
expression
mediators,
including
iNOS,
COX-2,
TNF-α,
IL-1β,
1L-6,
NOX-2,
NOX-4,
control
MP
vivo.
In
addition,
molecular
docking
experiments
that
had
high
affinity
SIRT1,
significantly
activated
SIRT1
PGC1α,
down-regulation
DRP1.
level
cellular
increased
potential,
which
improved
normal
After
administering
inhibitor
nicotinamide,
reversed.On
contrary,
agonist
SRT2183
further
enhanced
antioxidant
CAPE,
indicating
dependent
SIRT1.
Conclusion
inhibits
supports
regulating
pathway
These
demonstrate
reduces
nerve
damage.
Therefore,
is
drug
through
production
effects.
Graphical
Journal of Agricultural and Food Chemistry,
Год журнала:
2024,
Номер
72(32), С. 17964 - 17976
Опубликована: Авг. 3, 2024
Spinal
cord
injury
(SCI)
is
one
of
the
most
serious
health
problems,
with
no
effective
therapy.
Recent
studies
indicate
that
Fisetin,
a
natural
polyphenolic
flavonoid,
exhibits
multiple
functions,
such
as
life-prolonging,
antioxidant,
antitumor,
and
neuroprotection.
However,
restorative
effects
Fisetin
on
SCI
underlying
mechanism
are
still
unclear.
In
present
study,
we
found
reduced
LPS-induced
apoptosis
oxidative
damage
in
PC12
cells
reversed
M1
polarization
BV2
cells.
Additionally,
safely
effectively
promoted
motor
function
recovery
mice
by
attenuating
neurological
promoting
neurogenesis
at
lesion.
Moreover,
administration
inhibited
glial
scar
formation,
modulated
microglia/macrophage
polarization,
neuroinflammation.
Network
pharmacology,
RNA-seq,
molecular
biology
revealed
activation
JAK2/STAT3
signaling
pathway.
Notably,
Colivelin
TFA,
an
activator
signaling,
attenuated
Fis-mediated
neuroinflammation
inhibition
therapeutic
mice.
Collectively,
promotes
functional
after
inhibiting
Thus,
may
be
promising
drug
for
treatment
SCI.
Journal of Nanobiotechnology,
Год журнала:
2024,
Номер
22(1)
Опубликована: Авг. 12, 2024
The
secondary
injury
is
more
serious
after
traumatic
brain
(TBI)
compared
with
primary
injury.
Release
of
excessive
reactive
oxygen
species
(ROS)
and
Ca2+
influx
at
the
damaged
site
trigger
Herein,
a
neutrophil-like
cell
membrane-functionalized
nanoparticle
was
developed
to
prevent
ROS-associated
NCM@MP
composed
three
parts:
(1)
Differentiated
membrane
(NCM)
synthesized,
inflammation-responsive
ability
achieve
effective
targeting
increase
retention
time
Mn3O4
nimodipine
(MP)
in
deep
tissue
via
C-X-C
chemokine
receptor
type
4,
integrin
beta
1
macrophage
antigen-1.
(2)
Nimodipine
used
inhibit
influx,
eliminating
ROS
source.
(3)
further
eradicated
existing
ROS.
In
addition,
also
exhibited
desirable
properties
for
T1
enhanced
imaging
low
toxicity
which
may
serve
as
promising
multifunctional
nanoplatforms
precise
therapies.
our
study,
obviously
alleviated
oxidative
stress
response,
reduced
neuroinflammation,
protected
blood–brain
barrier
integrity,
relieved
edema,
promoted
regeneration
neurons,
improved
cognition
TBI
mice.
This
study
provides
management
relieve
spread
damage.
Pharmacological Research,
Год журнала:
2025,
Номер
212, С. 107578 - 107578
Опубликована: Янв. 5, 2025
Ginseng
has
been
commonly
used
as
a
traditional
Chinese
medicine
in
Asian
countries
for
thousands
of
years.
Ginsenosides
are
the
main
pharmacologically
active
ingredients
isolated
from
ginseng
and
have
neuroprotective
effects
treatment
neurodegenerative
disorders,
such
Parkinson's
disease
(PD)
Alzheimer's
(AD).
To
summarise
investigate
protective
roles
ginsenosides
their
underlying
mechanisms
PD
AD,
we
''Ginsenoside",
''Parkinson's
disease",
''Alzheimer's
''anti-inflammatory",
''antioxidant",
''apoptosis"
keywords
to
search
extract
relevant
literature
information
scientific
databases
Elsevier,
PubMed,
Google
Scholar
databases.
In
particular,
network
pharmacology
identify
potential
targets
Rg1
Rb1
AD.
By
analysing
existing
research
advances
results,
found
that
ginsenosides,
primarily
mediated
through
anti-inflammation,
anti-apoptosis
anti-oxidative
stress,
etc,
may
be
associated
with
PI3K/Akt,
BDNF/TrkB,
MAPKs,
NF-κB,
Nrf2
Wnt/β-catenin
signalling
pathways.
This
review
systematically
summarises
different
Rg1,
Rb1,
rare
AD
provides
new
strategies
disorders.
Network
paradigm
using
Rb1.
