Ecotoxicology and Environmental Safety,
Journal Year:
2024,
Volume and Issue:
287, P. 117305 - 117305
Published: Nov. 1, 2024
Arsenic
exposure
has
long
been
a
significant
global
health
concern
due
to
its
association
with
various
human
diseases.
The
adverse
effects
of
arsenic
can
be
influenced
by
multiple
factors,
resulting
in
considerable
individual
variability.
Individuals
inflammatory
bowel
disease
(IBD)
are
particularly
vulnerable
the
toxin
exposure,
yet
specific
impact
context
IBD
remains
unclear.
In
this
study,
we
employed
non-targeted
metabolomics
approach
investigate
how
affects
metabolic
homeostasis
an
model
using
Helicobacter
trogontum-infected
interleukin-10
deficient
mice.
Our
results
demonstrated
that
disrupted
balance
metabolites,
including
tryptophan,
polyunsaturated
fatty
acids,
purine
and
pyrimidine
branched-chain
amino
mice
colitis
but
not
those
without
colitis.
Notably,
several
crucial
metabolites
involved
anti-inflammatory
responses,
oxidative
stress,
energy
metabolism
were
significantly
altered
These
indicate
lead
extensive
disturbances,
potentially
exacerbating
severity
impacting
overall
health.
This
study
underscores
necessity
evaluating
toxicity
relation
better
understand
mitigate
associated
risks.
Journal of Agricultural and Food Chemistry,
Journal Year:
2024,
Volume and Issue:
72(28), P. 15985 - 15997
Published: July 3, 2024
Liver
disease
has
become
an
important
risk
factor
for
global
health.
Resveratrol
(Res)
is
a
natural
polyphenol
which
widely
found
in
foods
and
variety
of
biological
activities.
This
study
investigated
the
role
microbiota-gut-liver
axis
Res
relieving
liver
fibrosis
induced
by
inorganic
mercury
exposure.
Twenty-eight
mice
were
divided
into
four
groups
(n
=
7)
treated
with
mercuric
chloride
and/or
24
weeks,
respectively.
The
results
showed
that
mitigated
ileum
injury
restrained
LPS
alcohol
entering
body
circulation.
Network
pharmacological
molecular
analyses
alleviated
oxidative
stress,
metabolism
disorders,
inflammation,
hepatic
stellate
cell
activation
liver.
In
conclusion,
alleviates
via
activating
Sirt1/PGC-1α
signaling
pathway
regulating
microbial-gut-liver
axis,
particularly,
increasing
relative
enrichment
Bifidobacterium
intestinal
tract.
Toxicology,
Journal Year:
2024,
Volume and Issue:
503, P. 153767 - 153767
Published: March 1, 2024
Ricin
is
a
highly
toxic
plant
toxin
that
can
cause
multi-organ
failure,
especially
liver
dysfunction,
and
potential
bioterrorism
agent.
Despite
the
serious
public
health
challenge
posed
by
ricin,
effective
therapeutic
for
ricin-induced
poisoning
currently
unavailable.
Therefore,
it
important
to
explore
mechanism
of
ricin
develop
appropriate
treatment
protocols
accordingly.
Previous
studies
have
shown
lipid
peroxidation
iron
accumulation
are
associated
with
poisoning.
Ferroptosis
an
iron-dependent
form
cell
death
caused
excessive
peroxide.
The
role
ferroptosis
in
unclear
require
further
study.
We
investigated
effect
on
injury
elucidated
mechanism.
results
showed
occurred
ricin-intoxicated
rats,
Ferrostatin‑1
could
ameliorate
hepatic
thus
injury.
induced
decreasing
reduced
glutathione
protein
level
peroxidase
4
Solute
Carrier
Family
7
Member
11,
increasing
iron,
malondialdehyde
reactive
oxygen
species,
mitochondrial
damage,
whereas
pretreatment
increased
decreased
malondialdehyde,
ameliorated
thereby
alleviated
These
suggested
exacerbated
after
inhibition
may
be
novel
strategy
Food Frontiers,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Feb. 25, 2025
ABSTRACT
The
mechanism
of
anthocyanin
in
alleviating
intestine
injury
pigs
is
worth
pursuing
due
to
the
higher
similarity
physiological
structure
between
human
beings
and
than
rodents.
Herein,
we
investigated
by
which
improves
gut
damage
induced
with
lipopolysaccharide
further
confirmed
this
using
fecal
microbiota
transplantation.
Thirty‐two
piglets
were
randomly
divided
into
four
treatments:
control
group
(Control),
model
(LPS),
prophylactic
(An‐LPS),
transplantation
(FMT‐LPS).
results
showed
that
oxidative
stress
increased
expression
p‐p65,
Bax,
Keap1
decreased
Nrf2,
Occludin,
Claudin‐1
jejunum.
However,
its
suspension
reversed
these
influences.
Meanwhile,
selectively
improved
certain
microbiota,
including
Lactococcus
,
leading
distinct
metabolic
profiles.
These
differences
favor
activating
antioxidant‐related
signaling
pathway,
Nrf2/Keap1
inhibiting
pro‐inflammatory
pathway
such
as
NF‐κB,
alleviated
inflammation
significantly
intestinal
tight
junction,
Occludin
Claudin‐1.
Moreover,
compared
LPS,
serum
antioxidant
enzyme
activity
IL‐10
content
An‐LPS.
In
conclusion,
ameliorated
through
antioxidant‐
inflammation‐related
pathways;
meanwhile,
metabolites
play
a
nonsubstitutable
role
process.
Journal of Biochemical and Molecular Toxicology,
Journal Year:
2025,
Volume and Issue:
39(3)
Published: March 1, 2025
ABSTRACT
Resveratrol
alleviates
liver
fibrosis
in
mice
by
upregulating
IL‐10
to
reprogram
the
macrophage
phenotype;
however,
mechanism
remains
be
elucidated.
Building
on
our
previous
work,
this
study,
we
aimed
determine
role
of
TLR2/MyD88/ERK
and
NF‐κB/NLRP3
inflammasome
pathways
mediating
effects
resveratrol
polarization.
We
investigated
expression
cytokines
these
a
mouse
model
resveratrol‐treated
macrophages.
The
results
showed
that
TLR2,
MyD88,
ERK,
NF‐κB1
tissues
was
increased
fourth
week
after
treatment
with
but
decreased
fifth
week.
Similar
were
obtained
for
pathway.
also
both
macrophages
elevated
24
h
reduced
36
resveratrol.
Immunofluorescence
nucleocytoplasmic
separation
assays
inhibited
translocation
NF‐κB
from
cytoplasm
nucleus
macrophages,
associated
inhibition
Silencing
ERK.
In
conclusion,
are
involved
effect
polarization
subsequent
modulation
fibrosis.
acts
as
common
cytokine
coordinates
crosstalk
between
two
pathways.
Our
findings
highlight
potential
members
therapeutic
targets
toward
