Journal of Agricultural and Food Chemistry,
Год журнала:
2023,
Номер
71(14), С. 5450 - 5462
Опубликована: Апрель 3, 2023
Perfluorooctanesulfonic
acid
(PFOS),
a
fluorine-containing
organic
compound,
can
be
widely
detected
in
the
environment
and
living
organisms.
Accumulating
evidence
has
shown
that
PFOS
breaks
through
different
biological
barriers
resulting
cardiac
toxicity,
but
underlying
molecular
mechanisms
remain
unclear.
Cannabidiol
(CBD)
is
nonpsychoactive
cannabinoid
without
potential
adverse
cardiotoxicity
antioxidant
anti-inflammatory
properties
reduce
multiorgan
damage
dysfunction.
For
these
reasons,
aim
of
this
study
was
to
research
how
caused
heart
injury
whether
CBD
could
attenuate
PFOS-induced
injury.
Mice
were
fed
(5
mg/kg)
and/or
(10
vivo.
In
vitro,
H9C2
cells
intervened
with
(200
μM)
μM).
After
exposure,
oxidative
stress
levels
mRNA
protein
expression
apoptosis-related
markers
increased
distinctly,
accompanied
by
mitochondrial
dynamic
imbalance
energy
metabolism
disorders
mouse
cells.
Moreover,
terminal
deoxynucleotidyl
transferase
dUTP
nick
end
labeling
staining,
acridine
orange/ethidium
bromide
staining
Hoechst
33258
signaled
number
apoptotic
after
exposure
PFOS.
Noteworthy,
simultaneous
treatment
alleviated
series
damages
PFOS-mediated
stress.
Our
results
demonstrated
alleviate
dynamics
disorder
causing
cardiomyocyte
apoptosis
improving
capacity,
suggesting
may
represent
novel
cardioprotective
strategy
against
cardiotoxicity.
findings
facilitate
understanding
cardiotoxic
effects
important
role
protecting
health.
Environmental Toxicology,
Год журнала:
2023,
Номер
38(7), С. 1651 - 1664
Опубликована: Март 29, 2023
Perfluorooctane
sulfonate
(PFOS)
is
one
of
the
persistent
organic
pollutants
(POPs),
which
can
cause
severe
nephrotoxicity
in
mammals.
Cannabinol
(CBD),
a
nonpsychoactive
cannabinoid
obtained
from
cannabis
plant,
has
attracted
attention
recent
years
for
its
excellent
antioxidant
properties.
NADPH
oxidase
4
(NOX4)
an
important
effect
supporting
normal
renal
physiological
function.
The
potential
mechanisms
PFOS
and
whether
CBD
prevent
damage
caused
by
remain
unclear.
This
work
aimed
to
study
PFOS-induced
kidney
protective
role
against
damage.
We
demonstrated
that
led
insufficiency
structural
mice,
induced
overexpression
NOX4
onset
oxidative
stress,
activated
apoptosis
mitochondrial
pathway
via
JNK
signaling
pathway.
However,
treatment
with
reversed
these
changes.
For
further
investigation
mechanism
cell
apoptosis,
expression
was
inhibited
vitro
experiments
using
Apocynin,
effective
inhibitor.
outcomes
showed
ROS
production
activation
human
embryonic
(HEK293)
cells
were
significantly
reduced
after
inhibition
NOX4.
suggests
serves
as
upstream
event
activation.
In
conclusion,
findings
suggest
induces
NOX4/ROS/JNK
Meanwhile,
alleviated
through
axis
