Frontiers in Pharmacology,
Journal Year:
2023,
Volume and Issue:
14
Published: Oct. 17, 2023
Ischemic-induced
neuronal
injury
arises
due
to
low
oxygen/nutrient
levels
and
an
inflammatory
response
that
exacerbates
loss.
NOD-like
receptor
family
pyrin
domain-containing
3
(NLRP3)
is
important
regulator
of
inflammation
after
ischemic
stroke,
with
its
inhibition
being
involved
in
nerve
regeneration.
Curcumin,
a
main
active
ingredient
Chinese
herbs,
plays
positive
role
repair
neuroprotection
by
regulating
the
NLRP3
signaling
pathway.
Nevertheless,
mechanisms
relating
how
curcumin
regulates
inflammasome
neural
restoration
following
stroke
are
unknown.
In
this
report,
we
summarize
biological
functions
along
neuroprotective
effects
underlying
via
impairment
pathway
brain
injury.
We
also
discuss
medicinal
interventions
target
potential
pathways,
as
well
possible
directions
for
therapy
penetrate
blood-brain
barrier
(BBB)
hinder
stroke.
This
report
conclusively
demonstrates
has
properties
inhibit
prevent
cell
loss,
thereby
delaying
progression
damage.
Journal of Enzyme Inhibition and Medicinal Chemistry,
Journal Year:
2024,
Volume and Issue:
39(1)
Published: Feb. 29, 2024
Pterostilbene
(PST)
is
a
naturally
derived
stilbene
compound
in
grapes,
blueberries,
and
other
fruits.
It
also
natural
dietary
with
wide
range
of
biological
activities
such
as
antioxidant,
anti-inflammatory,
antitumor,
so
on.
Structural
modifications
based
on
the
chemical
scaffold
pterostilbene
skeleton
are
great
importance
for
drug
discovery.
In
this
study,
skeletons
were
used
to
design
novel
anti-inflammatory
compounds
high
activity
low
toxicity.
A
total
30
new
found
synthesised,
their
safety
screened.
Among
them,
E2
was
most
active
(against
NO:
IC50
=
0.7
μM)
than
celecoxib.
Further
studies
showed
that
exerted
by
blocking
LPS-induced
NF-κB/MAPK
signalling
pathway
activation.
vivo
experiments
revealed
had
good
alleviating
effect
acute
colitis
mice.
conclusion,
may
be
promising
lead
compound.
Renal Failure,
Journal Year:
2024,
Volume and Issue:
46(1)
Published: April 7, 2024
Acute
kidney
injury
(AKI)
is
associated
with
a
high
mortality
rate.
Pathologically,
renal
ischemia/reperfusion
(RIRI)
one
of
the
primary
causes
AKI,
and
hypoxia-inducible
factor
(HIF)-1α
may
play
defensive
role
in
RIRI.
This
study
assessed
1α
(HIF-1α)-mediated
mitophagy
protection
against
RIRI
vitro
vivo.
The
human
tubular
cell
line
HK-2
was
used
to
assess
hypoxia/reoxygenation
(H/R)-induced
through
different
assays,
including
western
blotting,
immunofluorescence
staining,
terminal
deoxynucleotidyl
transferase-mediated
dUTP
nick
end
labeling
(TUNEL),
reactive
oxygen
species
(ROS)
measurement.
Additionally,
rat
model
established
for
evaluation
by
histopathology,
Doppler
ultrasound,
transmission
electron
microscopy
confirm
data.
selective
HIF-1α
inhibitor
LW6
reduced
H/R-induced
but
increased
apoptosis
ROS
production.
Moreover,
H/R
treatment
enhanced
expression
FUN14
domain-containing
1
(FUNDC1)
protein.
FUNDC1
overexpression
reversed
effects
on
altered
light
chain
3
(LC3)
BII
voltage-dependent
anion
channels
as
well
blocked
inhibition
cells.
Pretreatment
roxadustat,
novel
oral
inhibitor,
led
decreased
In
conclusion,
HIF-1α/FUNDC1
signaling
pathway
mediates
H/R-promoted
mitophagy,
whereas
this
protects
cells
from
thus
aggravating
apoptosis,
Accordingly,
roxadustat
protect
RIRI-related
AKI.
Frontiers in Pharmacology,
Journal Year:
2023,
Volume and Issue:
14
Published: Oct. 17, 2023
Ischemic-induced
neuronal
injury
arises
due
to
low
oxygen/nutrient
levels
and
an
inflammatory
response
that
exacerbates
loss.
NOD-like
receptor
family
pyrin
domain-containing
3
(NLRP3)
is
important
regulator
of
inflammation
after
ischemic
stroke,
with
its
inhibition
being
involved
in
nerve
regeneration.
Curcumin,
a
main
active
ingredient
Chinese
herbs,
plays
positive
role
repair
neuroprotection
by
regulating
the
NLRP3
signaling
pathway.
Nevertheless,
mechanisms
relating
how
curcumin
regulates
inflammasome
neural
restoration
following
stroke
are
unknown.
In
this
report,
we
summarize
biological
functions
along
neuroprotective
effects
underlying
via
impairment
pathway
brain
injury.
We
also
discuss
medicinal
interventions
target
potential
pathways,
as
well
possible
directions
for
therapy
penetrate
blood-brain
barrier
(BBB)
hinder
stroke.
This
report
conclusively
demonstrates
has
properties
inhibit
prevent
cell
loss,
thereby
delaying
progression
damage.