Redox Biology,
Journal Year:
2023,
Volume and Issue:
69, P. 102983 - 102983
Published: Dec. 5, 2023
Shank3,
a
key
molecule
related
to
the
development
and
deterioration
of
autism,
has
recently
been
found
downregulate
in
murine
brain
after
ischemia/reperfusion
(I/R).
Despite
this
discovery,
however,
its
effects
on
neuronal
injury
mechanism
underlying
remain
be
clarified.
To
address
this,
study,
based
genetically
modified
mice
models,
we
revealed
that
expression
Shank3
showed
time-dependent
change
hippocampal
neurons
I/R,
conditional
knockout
(cko)
resulted
aggravated
injuries.
The
protective
against
oxidative
stress
inflammation
I/R
were
achieved
through
direct
binding
STIM1
subsequent
proteasome-mediated
degradation
STIM1.
downregulation
induced
phosphorylation
downstream
Nrf2
Ser40,
which
subsequently
translocated
nucleus,
further
increased
antioxidant
genes
such
as
NQO1
HO-1
HT22
cells.
In
vivo,
study
confirmed
double
Stim1
alleviated
Shank3cko
mice.
conclusion,
present
demonstrated
interacts
with
inhibits
post-I/R
inflammatory
response
via
pathway.
This
interaction
can
potentially
contribute
promising
method
for
treatment.
The American Journal of Chinese Medicine,
Journal Year:
2024,
Volume and Issue:
52(01), P. 231 - 252
Published: Jan. 1, 2024
Berberine
has
been
demonstrated
to
alleviate
cerebral
ischemia/reperfusion
injury,
but
its
neuroprotective
mechanism
yet
be
understood.
Studies
have
indicated
that
ischemic
neuronal
damage
was
frequently
driven
by
autophagic/lysosomal
dysfunction,
which
could
restored
boosting
transcription
factor
EB
(TFEB)
nuclear
translocation.
Therefore,
this
study
investigated
the
pharmacological
effects
of
berberine
on
TFEB-regulated
signaling
in
neurons
after
stroke.
A
rat
model
stroke
and
a
ischemia
HT22
cells
were
prepared
using
middle
artery
occlusion
(MCAO)
oxygen-glucose
deprivation
(OGD),
respectively.
pre-administered
at
dose
100[Formula:
see
text]mg/kg/d
for
three
days
rats
90[Formula:
text][Formula:
text]M
12[Formula:
text]h.
24[Formula:
text]h
MCAO
2[Formula:
OGD,
penumbral
tissues
OGD
obtained
detect
cytoplasmic
TFEB,
key
proteins
pathway
examined
western
blot
immunofluorescence,
Meanwhile,
neuron
survival,
infarct
volume,
neurological
deficits
assessed
evaluate
therapeutic
efficacy.
The
results
showed
prominently
facilitated
TFEB
translocation,
as
increased
expression
well
cells.
Consequently,
both
autophagic
activity
lysosomal
capacity
simultaneously
augmented
injury.
However,
berberine-conferred
neuroprotection
greatly
counteracted
inhibitor
Bafilomycin
A1
(Baf-A1).
autophagy
3-Methyladenine
(3-MA)
also
slightly
neutralized
effect
ameliorating
dysfunction.
Our
suggests
berberine-induced
against
is
elicited
enhancing
flux
via
facilitation
translocation
neurons.
Redox Biology,
Journal Year:
2023,
Volume and Issue:
69, P. 102983 - 102983
Published: Dec. 5, 2023
Shank3,
a
key
molecule
related
to
the
development
and
deterioration
of
autism,
has
recently
been
found
downregulate
in
murine
brain
after
ischemia/reperfusion
(I/R).
Despite
this
discovery,
however,
its
effects
on
neuronal
injury
mechanism
underlying
remain
be
clarified.
To
address
this,
study,
based
genetically
modified
mice
models,
we
revealed
that
expression
Shank3
showed
time-dependent
change
hippocampal
neurons
I/R,
conditional
knockout
(cko)
resulted
aggravated
injuries.
The
protective
against
oxidative
stress
inflammation
I/R
were
achieved
through
direct
binding
STIM1
subsequent
proteasome-mediated
degradation
STIM1.
downregulation
induced
phosphorylation
downstream
Nrf2
Ser40,
which
subsequently
translocated
nucleus,
further
increased
antioxidant
genes
such
as
NQO1
HO-1
HT22
cells.
In
vivo,
study
confirmed
double
Stim1
alleviated
Shank3cko
mice.
conclusion,
present
demonstrated
interacts
with
inhibits
post-I/R
inflammatory
response
via
pathway.
This
interaction
can
potentially
contribute
promising
method
for
treatment.
