Identification of Key Genes in Esketamine’s Therapeutic Effects on Perioperative Neurocognitive Disorders via Transcriptome Sequencing
Drug Design Development and Therapy,
Год журнала:
2025,
Номер
Volume 19, С. 981 - 1000
Опубликована: Фев. 1, 2025
Esketamine
ameliorates
propofol-induced
brain
damage
and
cognitive
impairment
in
mice.
However,
the
precise
role
underlying
mechanism
of
esketamine
perioperative
neurocognitive
disorders
(PND)
remain
unclear.
Therefore,
this
study
aimed
to
investigate
key
genes
associated
with
PND
through
animal
modeling
transcriptome
sequencing.
The
present
established
a
mice
model
administered
intervention
model,
were
divided
into
control,
surgical
group,
group
esketamine.
Behavioral
assessments
conducted
using
Morris
water
maze
Y
paradigms,
while
sequencing
was
performed
on
hippocampal
samples
obtained
from
3
groups.
Differential
expression
analysis
weighted
gene
co-expression
network
(WGCNA)
data
identify
candidate
related
treating
PND.
Thereafter,
protein-protein
interaction
(PPI)
implemented
select
genes.
each
step
subjected
enrichment
analysis,
regulatory
for
constructed.
findings
demonstrated
successful
construction
our
indicated
that
exhibits
certain
therapeutic
efficacy
Ank1,
Cbln4,
L1cam,
Gap43,
Shh
designated
as
subsequent
analysis.
5
significantly
enriched
cholesterol
biosynthesis,
nonsense
mediated
decay
(NMD),
formation
pool
free
40s
subunits,
major
pathway
rRNA
processing
nucleolus
cytosol,
among
others.
Notably,
miRNAs,
mmu-mir-155-5p
mmu-mir-1a-3p,
functionally
co-regulated
L1cam.
We
uncovered
identified
(Ank1,
Shh)
contribute
its
effects,
providing
valuable
reference
further
mechanistic
studies
esketamine's
treatment
Язык: Английский
Serum proteomic changes related to residual impairment in remittent depression are associated with immune and inflammatory processes
Scientific Reports,
Год журнала:
2024,
Номер
14(1)
Опубликована: Окт. 18, 2024
Abstract
In
patients
with
major
depressive
disorder,
various
functional
areas
are
impaired,
negatively
impacting
the
quality
of
life.
Remission
can
restore
pre-depression
functions;
however,
some
may
still
have
residual
impairments.
Distinguishing
between
near-normal
recovery
and
impairment
helps
identify
those
at
a
high
risk
relapse
tailor
treatment.
Accordingly,
we
aimed
to
discover
validate
biomarkers
that
distinguish
in
remission
states
through
serum
proteome
analysis.
Pooled
individual
samples
from
three
groups
(depression
status,
status
impairment,
normal
recovery)
were
analyzed
using
liquid
chromatography-tandem
mass
spectrometry.
The
combination
four
proteins—antithrombin-III,
amyloid
A4
protein,
C1q
subcomponent
subunit
B,
P-component—was
selected
as
candidate
biomarker.
trend
protein
changes
suggests
complement
B
P-component
potential
for
distinguishing
impairment.
Changes
suggest
system
inflammation-related
immune
mechanisms
associated
remittent
disorder.
Язык: Английский