Frontiers in Cardiovascular Medicine,
Journal Year:
2022,
Volume and Issue:
9
Published: June 29, 2022
Chemotherapy
has
significantly
improved
cancer
survival
rates
at
the
cost
of
irreversible
and
frequent
cardiovascular
toxicity.
As
main
dose-dependent
adverse
effect,
cardiotoxic
effects
not
only
limit
usage
chemotherapeutic
agents,
but
also
cause
high
risk
severe
poor
prognoses
for
survivors.
Therefore,
it
is
great
significance
to
seek
more
effective
cardioprotective
strategies.
Some
nutrients
have
been
reported
diminish
cardiac
oxidative
damage
associated
with
chemotherapy.
However,
currently
available
evidence
unclear,
which
requires
a
rigorous
summary.
such,
we
conducted
systematic
review
all
demonstrated
whether
derived
from
food
could
prevent
cardiotoxicity
caused
by
chemotherapy.We
searched
Medline
(via
PubMed),
Embase
Cochrane
Library
inception
Nov
9,
2021
identify
studies
reporting
dietary
against
chemotherapy-related
cardiotoxicity.
We
performed
descriptive
summaries
on
included
studies,
used
forest
plots
demonstrate
various
nutrients.Fifty-seven
eligible
were
identified,
involving
53
animal
carried
rats
or
mice
four
human
in
patients.
Seven
types
recognized
including
polyphenols
(mainly
extracted
grapes,
grape
seeds,
tea),
allicin
form
garlic),
lycopene
tomatoes),
polyunsaturated
fatty
acids,
amino
acids
referring
glutamine),
coenzyme
Q10,
trace
elements
zinc
selenium).
Dietary
ameliorated
left
ventricular
dysfunctions
myocardial
stress
varying
degrees,
The
overall
bias
was
moderate
risk.The
results
indicated
that
might
be
potential
strategy
protect
system
exposed
are
urged
this
field.Systematic
Review
Registration:
https://inplasy.com/inplasy-2022-3-0015/.
Cardiovascular Toxicology,
Journal Year:
2023,
Volume and Issue:
23(1), P. 46 - 60
Published: Jan. 1, 2023
Cuprizone
(CPZ)
is
a
neurotoxic
agent
that
used
to
induce
demyelination
and
neurotoxicity
in
rats.
This
study
aimed
investigate
the
protective
potential
of
sulforaphane
(SF),
nuclear
factor
E2
related
(Nrf-2)
activator,
against
CPZ-induced
cardiotoxicity
hepatotoxicity.
Male
adult
Wistar
rats
(n
=
18)
were
fed
with
regular
diet
or
CPZ-contained
(0.2%)
for
four
weeks.
The
divided
into
three
groups
6):
negative
control
rats,
CPZ-exposed
CPZ
+
SF
treated
was
intraperitoneally
administrated
(2
mg/kg/day)
two
anti-inflammatory
anti-oxidative
functions
investigated
biochemically,
histologically,
immunohistochemically.
increased
serum
levels
cardiac
troponin
1
(CTn1),
aspartate
amino
transaminase
(AST),
alanine
(ALT),
alkaline
phosphatase
(ALP).
In
addition,
inflammatory
interferon-gamma
(IFN-γ),
pro-inflammatory
interleukin
1β
(IL-1β)
significantly
elevated.
Moreover,
administration
provoked
oxidative
stress
as
manifested
by
declined
total
antioxidant
capacity
(TAC),
well
as,
stimulated
lipid
peroxidation
decreased
catalase
activities
both
hepatic
tissues.
treatment
reversed
all
these
biochemical
alterations
through
exerting
activities,
this
supported
histopathological
investigations
SF-triggered
modulation
inflammation
strongly
associated
Nrf-2
activation,
evidenced
activated
immunoexpression
highlights
cardioprotective
hepatoprotective
via
activation
enhancing
function.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(11), P. 5833 - 5833
Published: May 27, 2024
Doxorubicin
is
an
effective
drug
for
cancer
treatment;
however,
cardiotoxicity
limits
its
use.
Cardiotoxicity
pathophysiology
multifactorial.
GLP-1
analogues
have
been
shown
to
reduce
oxidative
stress
and
inflammation.
In
this
study,
we
evaluated
the
effect
of
pretreatment
with
liraglutide
on
doxorubicin-induced
acute
cardiotoxicity.
A
total
60
male
Wistar
rats
were
allocated
into
four
groups:
Control
(C),
(D),
Liraglutide
(L),
+
(DL).
L
DL
received
subcutaneous
injection
0.6
mg/kg
daily,
while
C
D
saline
2
weeks.
Afterwards,
a
single
intraperitoneal
doxorubicin
20
mg/kg;
saline.
Forty-eight
hours
after
administration,
subjected
echocardiogram,
isolated
heart
functional
euthanasia.
Liraglutide-treated
ingested
significantly
less
food
gained
body
weight
than
animals
that
did
not
receive
drug.
Rats
lost
injection.
At
echocardiogram
doxorubicin-treated
had
systolic
diastolic
function
impairment.
Myocardial
catalase
activity
was
statistically
higher
in
rats.
protein
expression
tumor
necrosis
factor
alpha
(TNF-α),
phosphorylated
nuclear
factor-κB
(p-NFκB),
troponin
T,
B-cell
lymphoma
(Bcl-2)
lower,
NFκB/p-NFκB
ratio
TLR-4
OPA-1,
MFN-2,
DRP-1,
topoisomerase
2β
differ
between
groups
(p
>
0.05).
conclusion,
accompanied
by
decreased
Bcl-2
NFκB
increased
expression.
failed
improve
Scientific Reports,
Journal Year:
2025,
Volume and Issue:
15(1)
Published: Feb. 24, 2025
Doxorubicin
(DOXO)
is
a
powerful
anthracycline
chemotherapeutic
drug,
but
its
clinical
usage
has
been
limited
by
deleterious
effects
on
different
organs,
particularly
hepatotoxicity.
The
aim
of
this
study
was
to
establish
the
combined
aerobic
interval
training
(AIT)
and
curcumin
supplementation
mitigating
oxidative
damage
endoplasmic
reticulum
(ER)
stress-mediated
apoptosis
in
rat
model
DOXO-induced
Fifty-six
male
Sprague–Dawley
rats
were
randomly
split
into
six
groups:
control
(CON),
vehicle,
doxorubicin
(Dox),
+
(Dox-C),
AIT
(Dox-A),
(Dox-AC).
DOXO
intraperitoneally
injected
weekly
(4
mg/kg/week)
for
five
weeks.
Curcumin
(100
mg/kg/day)
min
at
80–90%
VO2max
intermitted
3
active
rest
65–75%
VO2max)
conducted
times
week
Finally,
hepatic
tissue
blood
samples
collected
assess
histopathological
changes,
liver
biomarkers,
protein
expression
stress,
ER
markers.
Tissue
sections
revealed
that
significantly
improved
hepatotoxicity
induced
DOXO,
as
evidenced
positive
alterations
serum
markers
(P
<
0.05).
Both
reduced
DOXO-triggered
damage,
0.05),
with
latter
showing
slightly
higher
effectiveness.
Consequently,
combination
exhibits
protective
against
chronic
demonstrating
relatively
greater
efficacy
increasing
antioxidant
capacity
reducing
stress
apoptosis.
Scientific Reports,
Journal Year:
2025,
Volume and Issue:
15(1)
Published: March 20, 2025
Natural
products
like
gallic
acid
(GA),
a
phenolic
compound,
and
glycyrrhetinic
(GLA),
pentacyclic
triterpene,
have
been
shown
to
exhibit
antioxidant,
ant-inflammatory,
hepatoprotective
properties.
This
study
aims
investigate
the
protective
effects
of
GA,
GLA
their
combination
explore
underlying
mechanisms
against
acute
liver
damage
induced
by
azithromycin
(AZM)
in
rats.
Seven
groups
male
Wistar
rats
were
used
namely
control,
GLA,
AZM,
AZM
+
GA
groups.
We
treated
for
21
days,
administering
at
50
mg/kg
one
week
prior
(30
mg/kg).
Serum
levels
aspartate
aminotransferase,
alanine
alkaline
phosphatase
AZM-induced
pre-treated
with
therapy
much
lower
than
those
group
Elevated
glutathione,
catalase,
superoxide
dismutase
preventive
demonstrated
that
combinations
notably
reduced
malondialdehyde
levels,
an
oxidative
stress
marker,
improving
antioxidant
system
Furthermore,
pro-inflammatory
cytokines,
such
as
tumor
necrosis
factor-α
nuclear
factor
kappa
beta
(NF-kB),
thus
reversing
hepatic
inflammation.
also
discovered
down-regulated
erythroid
2-related
2
(Nrf2),
its
normal
restored
post
treatments
suggesting
Nrf2
signaling
pathway-mediated
prevention
damage.
In
conclusion,
protected
injury
through
ability
inflammation
preventing
downregulation
upregulation
NF-kB.
After
determining
efficacy
safety
clinical
settings
future
studies,
could
potentially
make
useful
therapeutic
drugs
mitigate
hepatotoxicity.
Future Journal of Pharmaceutical Sciences,
Journal Year:
2025,
Volume and Issue:
11(1)
Published: April 14, 2025
Abstract
Background
Doxorubicin
(DOX)
has
long
been
a
foundational
drug
in
cancer
therapeutics.
Despite
its
proven
efficacy,
the
persistent
challenge
of
mitigating
associated
side
effects,
notably
hepatotoxicity
and
neurotoxicity,
underscores
necessity
for
intervention.
Luteolin
(LUT)
is
naturally
derived
flavonoid
with
spectrum
bioactive
characteristics,
involving
anti-apoptotic,
antioxidant,
anti-inflammatory,
anti-cancer
attributes.
This
study
investigates
possible
protective
effect
LUT
against
DOX-induced
focusing
on
modulation
endoplasmic
reticulum
(ER)
stress
pathways
miRNA
199a-
5p
expression.
Forty-eight
male
Sprague
Dawley
rats
were
assigned
to
six
groups:
control,
(200
mg/kg),
DOX
(3.5
mg/kg,
i.p.)
administered
twice
per
week
3
weeks,
three
treatment
groups
that
received
daily
oral
gavage
at
doses
50,
100,
200
mg/kg
weeks
alongside
DOX.
Results
Behavioral
assessments
revealed
best
improvements
co-treated
high
dose
paralleled
by
mitigation
neurodegeneration
cortex
hippocampal
areas
brain.
The
hepatoprotective
mg/kg)
demonstrated
notable
decrease
liver
enzymes
restoration
hepatocytic
architecture,
coupled
upregulation
miRNA-199a-5p
suppression
glucose-regulated
protein
78
(GRP78).
inhibited
ER
via
suppressing
inositol-requiring
enzyme
1
alpha
(IRE1α)/protein
kinase
R-like
(PERK)/eukaryotic
initiation
factor
2
(eIF2α)/activating
transcription
6
(ATF6)
axes,
thereby
inhibiting
apoptosis.
Conclusions
efficacious
alleviating
hepatic
injury
neurotoxicity
dampening
pathways.
Graphical
abstract
Frontiers in Pharmacology,
Journal Year:
2025,
Volume and Issue:
16
Published: April 17, 2025
Doxorubicin
(DOX)
has
received
widespread
attention
as
a
broad-spectrum
antitumor
drug.
However,
it
been
recognized
challenge
that
long-term
DOX
injections
can
lead
to
severe
cardiotoxicity.
There
are
numerous
interventions
DOX-induced
cardiotoxicity,
and
the
most
cost-effective
is
phytochemicals.
It
reported
phytochemicals
have
complex
diverse
biological
properties,
facilitating
mitigation
of
cardiotoxicity
pathological
mechanisms,
nod-like
receptor
family
pyrin
domain-containing
3
(NLRP3)
inflammasome-mediated
cardiomyocyte
pyroptosis
one
them.
This
review
initially
presents
an
overview
mechanisms
underlie
induced
by
DOX.
Subsequently,
we
present
comprehensive
elucidation
structure
activation
NLRP3
inflammasome.
Finally,
provide
detailed
summary
mitigate
influencing
expression
inflammasome
in
cardiomyocytes.