The
concept
that
the
gut
microbiota
plays
a
significant
role
in
maintaining
physiological
status
gastrointestinal
(GI)
system
is
supported
by
both
qualitative
and
quantitative
transformation
of
intestinal
flora
various
pathological
conditions,
as
revealed
research
studies.
A
relationship
between
cognitive
functioning
clearly
suggested
evidence
neuroinflammation
seen
neurodegenerative
illnesses
like
Parkinson's
Alzheimer's.
Many
factors
will
affect
or
influence
microbiota.
Dysbiosis
microbiome
linked
to
decreased
immune
response,
which
encourages
growth
skin
diseases
causes
hair-related
disturbances.
Gut
alteration
related
many
skins
disorders.
Gut-brain
cross-talk
has
significantly
improved
interaction
hormones.
Ayurveda
can
be
applied
cosmetics
balance
symbiosis
microbial
ecology
using
organic
plant
botanicals.
According
this
perspective,
non-pathological
aging
process
may
facilitated
modulating
microbiota,
considers
interdependence
products,
inflammation
mediators,
system.
It
also
help
contrast
advancement
degenerative
mechanisms.
Certain
investigations,
with
encouraging
outcomes,
have
already
characterized
elderly
people.
connection
aging,
plague
older
people
should
better
understood
through
future
research.
Frontiers in Pharmacology,
Год журнала:
2024,
Номер
15
Опубликована: Фев. 19, 2024
Introduction:
Nephrotoxicity
represents
a
major
complication
of
using
doxorubicin
(DOX)
in
the
management
several
types
cancers.
Increased
oxidative
stress
and
activation
inflammatory
mediators
play
outstanding
roles
development
DOX-induced
kidney
damage.
This
study
aimed
to
investigate
whether
two
pathways
incretin-based
therapy,
glucagon-like
peptide-1
receptor
agonist
(presented
as
semaglutide,
SEM)
dipeptidyl
peptidase-4
inhibitor
alogliptin,
ALO),
differentially
protect
against
nephrotoxicity
rats
clarify
underlying
molecular
mechanisms.
Methods:
Adult
male
were
divided
into
six
groups:
control
(received
vehicle),
DOX
(20
mg/kg,
single
I.P.
on
day
8),
+
ALO
mg/kg/day,
P.O.
for
10
days),
SEM
(12
μg/kg/day,
S.C.
ALO-alone,
SEM-alone
groups.
At
end
study,
animals
sacrificed
their
functions,
stress,
markers
assessed.
Kidney
sections
also
subjected
histopathological
examinations.
Results:
The
co-treatment
with
either
or
manifested
an
improvement
evidenced
by
lower
serum
concentrations
creatinine,
urea,
cystatin
C
compared
group.
Lower
levels
MDA,
higher
GSH,
increased
SOD
activity
observed
ALO-
SEM-treated
groups
than
those
administration
resulted
decreased
renal
expressions
sirtuin
1
(SIRT1)
Nrf2
NF-κB
TNF-α
expressions,
these
effects
ameliorated
treatment
SEM.
Discussion:
Co-treatment
showed
renoprotective
effect
that
was
mediated
antioxidant
anti-inflammatory
via
SIRT1/Nrf2/NF-κB/TNF-α
pathway.
fact
both
therapy
demonstrate
equally
positive
alleviating
damage
is
noteworthy.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(9), С. 4972 - 4972
Опубликована: Май 2, 2024
Since
we
aim
to
test
new
options
find
medication
for
cognitive
disorders,
have
begun
assess
the
effect
of
semaglutide
and
conduct
a
review
gathering
studies
that
attempted
this
purpose.
This
systematic
focuses
on
effects
semaglutide,
glucagon-like
peptide
1
receptor
agonist
(GLP-1
RA),
in
context
neurological
impairment.
Semaglutide,
synthetic
GLP-1
analog,
showcased
neuroprotective
beyond
metabolic
regulation.
It
mitigated
apoptosis
improved
dysfunction
cerebrovascular
disease,
suggesting
broader
implications
well-being.
Also,
highlighted
RAs’
positive
impact
olfactory
function
obese
individuals
with
type
2
diabetes,
neurodegenerative
multiple
sclerosis,
endotoxemia.
In
order
analyze
current
function,
literature
search
was
conducted
up
February
2024
two
online
databases,
MEDLINE
(via
PubMed)
Web
Science
Core
Collection,
as
well
various
websites.
Fifteen
mice
populations
cell
lines
were
included,
analyzed,
assessed
bias-specific
tools.
The
anti-apoptotic
properties
its
analogs
emphasized,
animal
models
line
demonstrating
enhanced
function.
While
promising,
limitations
include
fewer
studies,
highlighting
need
extensive
research,
particularly
human
population.
Even
though
seems
there
are
significant
limitations,
one
which
is
lack
subjects.
Therefore,
aims
gather
evidence.
Current Issues in Molecular Biology,
Год журнала:
2024,
Номер
46(6), С. 5929 - 5949
Опубликована: Июнь 13, 2024
Semaglutide
(SEM),
a
glucagon-like
peptide-1
receptor
agonist,
has
garnered
increasing
interest
for
its
potential
therapeutic
effects
in
neurodegenerative
disorders
such
as
Alzheimer’s
disease
(AD)
and
Parkinson’s
(PD).
This
review
provides
comprehensive
description
of
SEM’s
mechanism
action
preclinical
studies
these
debilitating
conditions.
In
animal
models
AD,
SEM
proved
beneficial
on
multiple
pathological
hallmarks
the
disease.
administration
been
associated
with
reductions
amyloid-beta
plaque
deposition
mitigation
neuroinflammation.
Moreover,
treatment
shown
to
ameliorate
behavioral
deficits
related
anxiety
social
interaction.
SEM-treated
animals
exhibit
improvements
spatial
learning
memory
retention
tasks,
evidenced
by
enhanced
performance
maze
navigation
tests
novel
object
recognition
assays.
Similarly,
PD,
demonstrated
promising
neuroprotective
through
various
mechanisms.
These
include
modulation
neuroinflammation,
enhancement
mitochondrial
function,
promotion
neurogenesis.
Additionally,
improve
motor
function
dopaminergic
neuronal
loss,
offering
disease-modifying
strategies.
Overall,
accumulating
evidence
from
suggests
that
holds
promise
approach
AD
PD.
Further
research
is
warranted
elucidate
underlying
mechanisms
translate
findings
into
clinical
applications
devastating
disorders.
Naunyn-Schmiedeberg s Archives of Pharmacology,
Год журнала:
2025,
Номер
unknown
Опубликована: Март 15, 2025
Abstract
Pre-existing
diabetes
raises
the
likelihood
of
Parkinson’s
disease
(PD),
according
to
epidemiological
and
animal
research.
Our
study
aimed
investigating
likely
neuroprotective
effect
metformin
(Met)
and/or
semaglutide
(Sem)
in
model
PD
male
diabetic
rats
possible
underlying
mechanism.
Type
2
(T2DM)
was
induced
by
giving
high-fat
diet
(HFD)
for
3
weeks
followed
a
single
streptozotocin
(STZ)
injection
(40
mg/kg,
i.p.,
once
dose)
9
doses
rotenone
every
48
±
h
induction
PD.
Met
Sema
were
administered
DM+PD
via
gastric
gavage
daily
4
weeks.
In
comparison
with
group,
Sem
significantly
lowered
blood
glucose
levels,
HOMA-IR,
HbA1C,
cholesterol,
triglycerides,
LDL
increased
insulin
HDL
levels.
addition,
there
enhanced
brain
antioxidant
status
lower
oxidative-inflammatory
stress
biomarkers
associated
improved
rat
cognitive,
locomotor,
olfactory
functions.
A
significant
downregulation
caspase
GFAP
concomitant
upregulation
NRF2
protein
expressions
observed
treated
groups.
Overall,
co-treatment
elicited
more
efficacy
than
that
individual
regimen.
When
combined,
results
this
have
demonstrated
first
time
work
concert
create
neuroprotection
compared
when
taken
separately.
The
study’s
findings
indicate
restorative
on
T2DM
PD-induced
changes
neurobehavioral
biochemical/molecular
indices
ascribed
improvement
endogenous
systems,
decreased
lipid
peroxidation,
suppression
oxidative/inflammatory
stress,
and—most
importantly—regulation
Nrf2
3.
Graphical
abstract
Drug Development Research,
Год журнала:
2023,
Номер
84(6), С. 1159 - 1174
Опубликована: Май 12, 2023
Growing
evidence
points
to
impaired
autophagy
as
one
of
the
major
factors
implicated
in
pathophysiology
Parkinson's
disease
(PD).
Autophagy
is
a
downstream
target
adenosine
monophosphate-activated
protein
kinase
(AMPK).
Inosine
has
already
demonstrated
neuroprotective
effect
against
neuronal
loss
neurodegenerative
diseases,
mainly
due
its
anti-inflammatory
and
antioxidant
properties.
We,
herein,
aimed
at
investigating
effects
inosine
rotenone-induced
PD
rats
focus
on
activation
AMPK-mediated
autophagy.
successfully
increased
p-AMPK/AMPK
ratio
improved
their
motor
performance
muscular
co-ordination
(assessed
by
rotarod,
open
field,
grip
strength
tests,
well
manual
gait
analysis).
Furthermore,
was
able
mitigate
histopathological
alterations
restore
tyrosine
hydroxylase
immunoreactivity
rats'
substantia
nigra.
Inosine-induced
AMPK
resulted
an
enhancement,
striatal
Unc-S1-like
kinase1
beclin-1
expression,
also
increment
light
chain
3II
3I
ratio,
along
with
decline
mammalian
rapamycin
p62
expressions.
The
inosine-induced
stimulation
attenuated
apoptosis
promoted
activity.
Unsurprisingly,
these
were
antagonized
preadministration
dorsomorphin
(an
inhibitor).
In
conclusion,
exerted
via
through
restoration
imbalance
between
apoptosis.
These
findings
support
potential
application
treatment.
Neural Regeneration Research,
Год журнала:
2023,
Номер
19(8), С. 1671 - 1677
Опубликована: Дек. 11, 2023
The
glucagon-like
peptide
1
is
a
pleiotropic
hormone
that
has
potent
insulinotropic
effects
and
key
in
treating
metabolic
diseases
such
as
diabetes
obesity.
Glucagon-like
exerts
its
by
activating
membrane
receptor
identified
many
tissues,
including
different
brain
regions.
activates
several
signaling
pathways
related
to
neuroprotection,
like
the
support
of
cell
growth/survival,
enhancement
promotion
synapse
formation,
autophagy,
inhibition
secretion
proinflammatory
cytokines,
microglial
activation,
apoptosis
during
neural
morphogenesis.
glial
cells,
astrocytes
microglia,
maintain
homeostasis
defense
against
pathogens
central
nervous
system.
After
insult,
microglia
are
first
cells
respond,
followed
reactive
astrocytosis.
These
activated
produce
mediators
cytokines
or
chemokines
react
insult.
Furthermore,
under
these
circumstances,
can
become
chronically
inflammatory
losing
their
homeostatic
molecular
signature
and,
consequently,
functions
diseases.
Several
processes
promote
development
neurological
disorders
influence
pathological
evolution:
formation
protein
aggregates,
accumulation
abnormally
modified
cellular
constituents,
release
injured
neurons
synapses
molecules
dampen
function,
critical
importance,
dysregulation
control
mechanisms.
agonist
emerges
tool
brain-related
pathologies,
restoring
conditions,
modulating
activity,
decreasing
response.
This
review
summarizes
recent
advances
linked
anti-inflammatory
properties
activation
multiple
sclerosis,
Alzheimer's
disease,
Parkinson's
vascular
dementia,
chronic
migraine.