Electroacupuncture Attenuates Intestinal Barrier Disruption via the α7nAChR-Mediated HO-1/p38 MAPK/NF-κB Pathway in a Mouse Model of Metabolic Dysfunction-Associated Fatty Liver Disease: A Randomized, Single-Blind, Controlled Trial
Biomedicines,
Год журнала:
2025,
Номер
13(4), С. 802 - 802
Опубликована: Март 27, 2025
Background:
Gut
barrier
integrity
plays
a
crucial
role
in
the
pathogenesis
of
metabolic
dysfunction-associated
fatty
liver
disease
(MAFLD).
Electroacupuncture
(EA)
at
ST-36
can
ameliorate
inflammatory
responses
via
stimulating
α7
nicotinic
acetylcholine
receptor
(α7nAChR),
but
whether
EA
is
effective
preserving
intestinal
MAFLD
has
not
been
exactly
illustrated.
This
investigation
explored
potential
protection
mechanisms
targeting
dismantled
gut
MAFLD.
Methods:
C57BL/6
mice
were
randomly
allocated
into
several
subgroups:
control
(CON),
high-fat
diet
(HFD),
HFD
with
EA,
and
α7nAChR
inhibitor
α-BGT,
HO-1
knockout
(KO).
Body
weight,
visceral
fat
index,
histopathological
examination
intestine
determined.
Serum
biological
indexes
evaluated
through
corresponding
kits.
Furthermore,
expressions
HO-1,
α7nAChR,
barrier-associated
proteins,
molecular
tissues
assessed
Western
blot,
RT-qPCR,
immunohistology,
or
immunofluorescence
examination.
Results:
treatment
decreased
body
index
gain
mitigated
function
injury
abnormal
lipid
indexes,
exhibiting
less
severity
hepatic
steatosis,
fibrosis,
inflammation
Lower
permeability,
epithelial
disruption,
upregulation
tight
junction
proteins
after
suggested
protective
effects
attenuating
dysfunction.
These
abolished
by
α-BGT
deletion.
Mechanistically,
markedly
enriched
expression
phosphorylated
p38
MAPK/NF-κB
activation,
which
was
lost
KO
treatment.
Conclusions:
The
may
be
attributed
to
preserved
barrier,
thereby
alleviating
systemic
preventing
subsequent
hits,
where
α7nAChR-mediated
HO-1/p38
pathway
maintain
homeostasis.
Язык: Английский
Electroacupuncture combined with HDAC1 inhibitor suppress tumor growth via improving the recruitment of intratumor CD8+ T cells for triple-negative breast cancer in mice
Frontiers in Oncology,
Год журнала:
2025,
Номер
15
Опубликована: Май 22, 2025
Triple-negative
breast
cancer
(TNBC)
is
known
for
its
aggressive
nature
and
poor
prognosis,
primarily
due
to
limited
treatment
options
stemming
from
immune
evasion
mechanisms.
This
study
aimed
explore
the
therapeutic
potential
of
peritumoral
electroacupuncture
(EA)
in
inhibiting
tumor
growth
TNBC,
particularly
focusing
on
mechanisms
related
CD8+
T
cell
recruitment
involvement
histone
deacetylase
1
(HDAC1)
within
microenvironment
(TME).
By
constructing
TNBC
model
mice,
we
observed
that
EA
not
only
inhibited
but
also
increased
presence
intratumoral
cells
CCL5.
Additionally,
expression
HDAC1
was
found
down-regulate
by
EA.
Remarkably,
when
combined
with
romidepsin
(a
class
I
HDAC
inhibitor),
a
synergistic
effect
observed,
leading
greater
increase
compared
either
alone,
resulting
inhibition
rate
60.03%.
Importantly,
did
worsen
systemic
inflammation,
as
serum
levels
pro-inflammatory
cytokines
remained
stable
throughout
intervention.
These
findings
indicate
can
effectively
enhance
anti-tumor
immunity
TME
down-regulating
HDAC1.
research
highlights
combining
non-invasive
therapies
like
pharmacological
agent
promising
strategy
improving
outcomes
management
warranting
further
exploration
clinical
applications.
Язык: Английский