Biomedicines,
Год журнала:
2024,
Номер
12(12), С. 2797 - 2797
Опубликована: Дек. 10, 2024
Background:
SGLT-2
inhibitors
(SGLT-2i)
and
GLP-1
receptor
agonists
(GLP-1RA)
have
demonstrated
nephro-
cardioprotective
effects,
but
their
neuroprotective
properties,
especially
concerning
stroke
severity,
mechanisms
are
not
unambiguous.
We
aimed
to
study
the
influence
of
SGLT-2i
with
different
selectivity
GLP-1RA
on
brain
damage
volume
neurological
status
in
non-diabetic
diabetic
rats
investigate
underlying
mechanisms.
Methods:
Non-diabetic
Wistar
were
divided
into
five
groups
(n
=
10
each)
received
empagliflozin,
canagliflozin,
or
dulaglutide
as
drugs
metformin
comparison
drug.
Control
animals
administered
0.9%
NaCl
for
7
days
before
stroke.
At
48
h
after
stroke,
we
assessed
deficit,
neuronal
astroglial
markers,
volume.
also
modeled
type
2
DM
using
high-fat
diet+nicotinamide/streptozotocin
method
established
similar
treatment
groups.
After
8
weeks,
subjected
further
neuroglial
necrosis
measurement.
Results:
In
rats,
all
showed
an
infarct-limiting
effect;
more
effective
than
metformin.
DULA
improved
compared
MET
treatment.
All
decreased
neurofilament
light
chains
(NLCs)
level
none
them
glial
marker
S100BB.
DM,
similarly,
had
effects.
Neurological
deficit
was
most
pronounced
untreated
reduced
by
drugs.
NLC
level;
None
affected
neuron-specific
enolase.
Conclusions:
experimental
might
be
conditions
it
influences
both
status.
decrease
damage,
while
highly
selective
EMPA,
low-selective
CANA,
impact
neuroglia
conditions.
Biomedicines,
Год журнала:
2024,
Номер
12(10), С. 2387 - 2387
Опубликована: Окт. 18, 2024
Within
the
central
nervous
system,
synaptic
plasticity,
fundamental
to
processes
like
learning
and
memory,
is
largely
driven
by
activity-dependent
changes
in
strength.
This
plasticity
often
manifests
as
long-term
potentiation
(LTP)
depression
(LTD),
which
are
bidirectional
modulations
of
efficacy.
Strong
epidemiological
experimental
evidence
show
that
heart-brain
axis
could
be
severely
compromised
both
neurological
cardiovascular
disorders.
Particularly,
disorders,
such
heart
failure,
hypertension,
obesity,
diabetes
insulin
resistance,
arrhythmias,
may
lead
cognitive
impairment,
a
condition
known
cardiogenic
dementia.
Herein,
we
review
available
knowledge
on
molecular
mechanisms
dementia
arise
describe
how
LTP
and/or
LTD
induction
maintenance
CA1
region
hippocampus
metabolic
syndrome,
arrhythmias.
We
also
discuss
emerging
endothelial
dysfunction
contribute
directly
altering
hippocampal
impairing
synaptically
induced
activation
nitric
oxide
synthase.
A
better
understanding
CV
disorders
impact
proper
function
synapses
will
shed
novel
light
underpinnings
dementia,
thereby
providing
new
perspective
for
more
specific
pharmacological
treatments.
Current Issues in Molecular Biology,
Год журнала:
2024,
Номер
46(11), С. 12417 - 12427
Опубликована: Ноя. 4, 2024
Sodium-glucose
cotransporter-2
(SGLT2)
inhibitors
regulate
blood
glucose
levels
in
patients
with
type
2
diabetes
mellitus
and
may
also
exert
anti-inflammatory
anti-atherosclerotic
effects
by
promoting
M2
macrophage
polarization.
Although
SGLT2
is
expressed
brain
regions
that
influence
balance
cognitive
function,
its
roles
the
central
nervous
system
are
unclear.
This
study
investigated
of
empagliflozin
(EMPA),
an
inhibitor,
on
hypothalamic
inflammation
associated
metabolic
diseases.
Mice
were
subjected
to
a
high-fat
diet
(HFD)
for
varying
durations
(3
d,
3
weeks,
16
weeks)
treated
EMPA
weeks
(NFD,
NFD
+
EMPA,
HFD,
HFD
EMPA;
Biomedicines,
Год журнала:
2024,
Номер
12(12), С. 2783 - 2783
Опубликована: Дек. 6, 2024
Type
2
diabetes
mellitus
(T2DM),
accounting
for
the
majority
of
prevalence,
is
associated
with
an
increased
risk
cognition
decline
and
deterioration
function
in
diabetic
patients.
The
sodium–glucose
cotransporter
(SGLT2),
located
renal
proximal
tubule,
plays
a
role
urine
glucose
reabsorption.
SGLT2
inhibitors
(SGLT2i),
have
shown
potential
benefits
beyond
cardiac
improvement
preventing
treating
cognitive
impairment
(CI),
including
mild
impairment,
Alzheimer’s
disease
vascular
dementia
T2DM
Studies
suggest
that
SGLT2i
may
ameliorate
CI
through
metabolism
pathways,
inflammation,
oxidative
stress,
neurotrophic
factors
AChE
inhibition.
Clinical
trials
meta-analyses
reported
significant
insignificant
results.
Given
their
effects,
offer
unique
protection
against
CI.
This
review
compiles
mechanisms
clinical
evidence,
emphasizing
need
future
analysis,
evaluation,
to
verify
recommend
optimal
selection
dosage
specific
Biomedicines,
Год журнала:
2024,
Номер
12(12), С. 2797 - 2797
Опубликована: Дек. 10, 2024
Background:
SGLT-2
inhibitors
(SGLT-2i)
and
GLP-1
receptor
agonists
(GLP-1RA)
have
demonstrated
nephro-
cardioprotective
effects,
but
their
neuroprotective
properties,
especially
concerning
stroke
severity,
mechanisms
are
not
unambiguous.
We
aimed
to
study
the
influence
of
SGLT-2i
with
different
selectivity
GLP-1RA
on
brain
damage
volume
neurological
status
in
non-diabetic
diabetic
rats
investigate
underlying
mechanisms.
Methods:
Non-diabetic
Wistar
were
divided
into
five
groups
(n
=
10
each)
received
empagliflozin,
canagliflozin,
or
dulaglutide
as
drugs
metformin
comparison
drug.
Control
animals
administered
0.9%
NaCl
for
7
days
before
stroke.
At
48
h
after
stroke,
we
assessed
deficit,
neuronal
astroglial
markers,
volume.
also
modeled
type
2
DM
using
high-fat
diet+nicotinamide/streptozotocin
method
established
similar
treatment
groups.
After
8
weeks,
subjected
further
neuroglial
necrosis
measurement.
Results:
In
rats,
all
showed
an
infarct-limiting
effect;
more
effective
than
metformin.
DULA
improved
compared
MET
treatment.
All
decreased
neurofilament
light
chains
(NLCs)
level
none
them
glial
marker
S100BB.
DM,
similarly,
had
effects.
Neurological
deficit
was
most
pronounced
untreated
reduced
by
drugs.
NLC
level;
None
affected
neuron-specific
enolase.
Conclusions:
experimental
might
be
conditions
it
influences
both
status.
decrease
damage,
while
highly
selective
EMPA,
low-selective
CANA,
impact
neuroglia
conditions.
