Journal of Neuroinflammation,
Год журнала:
2021,
Номер
18(1)
Опубликована: Дек. 1, 2021
Stress-induced
neuroinflammation
was
considered
to
play
a
critical
role
in
the
pathogenesis
of
depression.
Transcutaneous
auricular
vagus
nerve
stimulation
(taVNS)
is
relatively
non-invasive
alternative
treatment
for
patients
suffering
from
major
depressive
disorder.
The
anti-inflammatory
signal
mediated
by
α7
nicotinic
acetylcholine
receptor
(α7nAchR),
and
hippocampus,
region
with
most
distribution
α7nAchR,
regulates
emotions.
Here,
we
investigated
α7nAchR
mediating
hippocampal
taVNS
antidepressant
effect
though
homozygous
α7nAChR
(-/-)
gene
knockout
antagonist
(methyllycaconitine,
MLA).There
were
control,
model,
taVNS,
α7nAChR(-/-)
+
hippocampus
(Hi)
MLA
Hi
saline
groups.
We
used
chronic
unpredicted
mild
stress
(CUMS)
method
establish
model
rats
42
days,
excepting
control
group.
After
successful
modeling,
except
other
groups
given
which
applied
through
an
electroacupuncture
apparatus
at
concha
(2/15
Hz,
2
mA,
30
min/days)
21
days.
Behavioral
tests
conducted
baseline,
after
modeling
intervention,
including
sucrose
preference
test
(SPT),
open
field
(OFT)
forced
swimming
(FST).
These
are
widely
evaluate
depression-like
behavior
rats.
samples
taken
experiment,
expressions
NF-κB
p65,
IL-1β
morphology
microglia
detected.Depression-like
CUMS
manifested
down-regulated
expression
up-regulated
p65
IL-1β,
amoebic-like
activated
state.
TaVNS
could
significantly
reverse
above-mentioned
phenomena,
but
had
rare
improvement
rats.The
related
α7nAchR/NF-κB
pathway.
Reviews in the Neurosciences,
Год журнала:
2018,
Номер
30(2), С. 179 - 201
Опубликована: Сен. 2, 2018
Here
we
offer
a
review
of
the
evidence
for
hypothesis
that
combination
ingestible
probiotics,
prebiotics,
postbiotics,
and
amino
acids
will
help
ameliorate
dysbiosis
degeneration
gut,
therefore
promote
restoration
nervous
system
function
in
number
neurological
indications.
Frontiers in Neurology,
Год журнала:
2019,
Номер
10
Опубликована: Авг. 16, 2019
Current
efficacious
treatments
for
traumatic
brain
injury
(TBI)
are
lacking.
Establishment
of
a
protective
gut
microbiota
population
offers
compelling
therapeutic
avenue,
as
induces
disruptions
in
the
composition
microbiota,
i.e.
dysbiosis,
which
has
been
shown
to
contribute
TBI-related
neuropathology
and
impaired
behavioral
outcomes.
The
microbiome
is
involved
modulation
multitude
cellular
molecular
processes
fundamental
progression
TBI-induced
pathologies
including
neuroinflammation,
blood
barrier
permeability,
immune
system
response,
microglial
activation,
mitochondrial
dysfunction,
well
intestinal
motility
permeability.
Additionally,
dysbiosis
further
aggravates
impairments
animal
models
TBI
spinal
cord
injury,
negatively
affects
health
outcomes
murine
stroke
models.
Recent
studies
indicate
that
transplants
probiotics
ameliorate
neuroanatomical
damage
functional
injury.
In
addition,
have
reduce
rate
infection
time
spent
intensive
care
hospitalized
patients
suffering
from
trauma.
Perturbations
its
metabolite
profile
may
also
serve
potential
diagnostic
theragnostic
biomarkers
severity
progression.
This
review
aims
address
etiological
role
biochemical,
neuroanatomical,
behavioral/cognitive
consequences
TBI,
explore
manipulation
form
an
effective
pathology
symptoms.
Journal of Neuroinflammation,
Год журнала:
2021,
Номер
18(1)
Опубликована: Дек. 1, 2021
Stress-induced
neuroinflammation
was
considered
to
play
a
critical
role
in
the
pathogenesis
of
depression.
Transcutaneous
auricular
vagus
nerve
stimulation
(taVNS)
is
relatively
non-invasive
alternative
treatment
for
patients
suffering
from
major
depressive
disorder.
The
anti-inflammatory
signal
mediated
by
α7
nicotinic
acetylcholine
receptor
(α7nAchR),
and
hippocampus,
region
with
most
distribution
α7nAchR,
regulates
emotions.
Here,
we
investigated
α7nAchR
mediating
hippocampal
taVNS
antidepressant
effect
though
homozygous
α7nAChR
(-/-)
gene
knockout
antagonist
(methyllycaconitine,
MLA).There
were
control,
model,
taVNS,
α7nAChR(-/-)
+
hippocampus
(Hi)
MLA
Hi
saline
groups.
We
used
chronic
unpredicted
mild
stress
(CUMS)
method
establish
model
rats
42
days,
excepting
control
group.
After
successful
modeling,
except
other
groups
given
which
applied
through
an
electroacupuncture
apparatus
at
concha
(2/15
Hz,
2
mA,
30
min/days)
21
days.
Behavioral
tests
conducted
baseline,
after
modeling
intervention,
including
sucrose
preference
test
(SPT),
open
field
(OFT)
forced
swimming
(FST).
These
are
widely
evaluate
depression-like
behavior
rats.
samples
taken
experiment,
expressions
NF-κB
p65,
IL-1β
morphology
microglia
detected.Depression-like
CUMS
manifested
down-regulated
expression
up-regulated
p65
IL-1β,
amoebic-like
activated
state.
TaVNS
could
significantly
reverse
above-mentioned
phenomena,
but
had
rare
improvement
rats.The
related
α7nAchR/NF-κB
pathway.
