Synergistic Neuroprotection Through Epigenetic Modulation by Combined Curcumin-Enriched Turmeric Extract and L-Ascorbic Acid in Oxidative Stress-Induced SH-SY5Y Cell Damage
Foods,
Journal Year:
2025,
Volume and Issue:
14(5), P. 892 - 892
Published: March 5, 2025
Epigenetic
modulation
plays
a
crucial
role
in
neuroprotection
by
regulating
cellular
responses
to
stress,
inflammation,
and
oxidative
damage,
particularly
neurodegenerative
diseases.
Recognizing
the
therapeutic
potential
of
epigenetic
regulators,
this
study
investigated
synergistic
neuroprotective
effects
curcumin-enriched
turmeric
extract
combined
with
L-ascorbic
acid,
focusing
on
its
pathways
stress-induced
neuronal
damage.
SH-SY5Y
cells
were
treated
combination
at
20
40
µg/mL,
subsequently
exposed
200
µM
hydrogen
peroxide
(H2O2)
induce
stress.
Cell
viability
was
assessed
using
MTT
assay,
while
mechanisms
evaluated
analyzing
markers
modulation,
apoptosis.
The
significantly
enhanced
cell
viability,
upregulated
sirtuin-1
(SIRT1),
reduced
DNA
methyltransferase
1
(DNMT1)
expression,
indicating
effective
modulation.
Enhanced
antioxidant
defenses
observed,
as
evidenced
increased
activities
superoxide
dismutase
(SOD),
catalase
(CAT),
glutathione
peroxidase
(GSH-Px),
along
decreased
malondialdehyde
(MDA)
reactive
oxygen
species
(ROS)
levels,
alleviating
Additionally,
it
suppressed
nuclear
factor
kappa
B
(NF-κB)
activity
downstream
mediator
interleukin-6
(IL-6),
thereby
mitigating
inflammation.
treatment
also
anti-apoptotic
Bcl-2
expression
reducing
pro-apoptotic
markers,
including
caspase-3
caspase-9,
suggesting
inhibition
intrinsic
apoptotic
pathway.
These
findings
highlight
novel
combination,
demonstrating
ability
modulate
suppressing
preventing
undesired
Its
multifaceted
properties
make
promising
functional
ingredient
foods
for
disease
intervention.
However,
further
investigations,
animal
studies
clinical
trials,
are
essential
evaluate
safety
potential.
Language: Английский
Role of Natural Compounds Modulating Heme Catabolic Pathway in Gut, Liver, Cardiovascular, and Brain Diseases
Biomolecules,
Journal Year:
2024,
Volume and Issue:
14(1), P. 63 - 63
Published: Jan. 2, 2024
The
crucial
physiological
process
of
heme
breakdown
yields
biliverdin
(BV)
and
bilirubin
(BR)
as
byproducts.
BV,
BR,
the
enzymes
involved
in
their
production
(the
“yellow
players—YP”)
are
increasingly
documented
endogenous
modulators
human
health.
Mildly
elevated
serum
concentration
has
been
correlated
with
a
reduced
risk
multiple
chronic
pro-oxidant
pro-inflammatory
diseases,
especially
elderly.
BR
BV
per
se
have
demonstrated
to
protect
against
neurodegenerative
which
oxygenase
(HMOX),
main
enzyme
pigments,
is
almost
always
altered.
HMOX
upregulation
interpreted
tentative
defense
ongoing
pathologic
mechanisms.
With
demonstration
that
cells
possess
YP,
propensity
be
modulated,
broad
spectrum
activity
on
signaling
pathways,
YP
assumed
role
an
adjustable
system
can
promote
health
adults.
Based
that,
there
effort
induce
therapeutic
option,
natural
compounds
attractive
alternative
goal,
possibly
requiring
only
minimal
changes
life
style.
We
review
most
recent
evidence
potential
targeting
context
common
condition
adult
elderly
life.
Language: Английский
Focusing on Keap1, IKKβ, and Bcl2 proteins: predicted targets of stigmasterol in neurodegeneration
Journal of Receptors and Signal Transduction,
Journal Year:
2025,
Volume and Issue:
unknown, P. 1 - 12
Published: Feb. 13, 2025
Oxidative
stress,
driven
by
excess
ROS,
damages
lipids,
proteins,
and
DNA,
leading
to
neuronal
apoptosis
inflammation,
a
key
factor
in
neurodegenerative
diseases.
This
study
explored
stigmasterol,
bioactive
phytosterol,
with
neuroprotective
potential,
revealing
strong
docking
interactions,
especially
Keap1
(binding
energy
of
−11.62
Kcal/mol).
Stigmasterol
formed
two
hydrogen
bonds
Ile258
Val305
Keap1,
suggesting
it
could
disrupt
Keap1-Nrf2
potentially
activating
antioxidant
responses
promoting
Nrf2
translocation
the
nucleus.
In
Bcl2-stigmasterol
complex,
which
exhibited
binding
−8.41
Kcal/mol,
hydrophobic
interactions
residues
Ser50,
Gln52,
Leu185
stabilized
indicating
stigmasterol's
role
inhibiting
strengthening
Bcl2
mediated
inhibition
pro-apoptotic
factors
like
Bax.
Furthermore,
IKKβ-stigmasterol
complex
displayed
bond
between
Asp385
residue
stigmasterol
(2.83
Å),
−8.33
suggested
that
may
regulate
inflammation
stabilizing
IKKβ,
thereby
preventing
NF-κB
reducing
inflammation.
Molecular
dynamics
simulations
confirmed
stability
showed
low
RMSD
values
consistent
bonding.
RMSF
Rg
analyses
indicated
had
effects
on
IKKβ.
These
results
underscore
potential
for
neuroprotection
through
anti-inflammatory
actions.
Language: Английский
Benchmark doses (BMD) extrapolated from in vitro cytotoxicity experiments in SH-SY5Y cells using the EFSA Bayesian BMD web app: The study case of imidacloprid
Computational Toxicology,
Journal Year:
2025,
Volume and Issue:
unknown, P. 100346 - 100346
Published: April 1, 2025
Language: Английский
Pharmacotherapeutic potential of malvidin to cure imidacloprid induced hepatotoxicity via regulating PI3K/AKT, Nrf-2/Keap-1 and NF-κB pathway
H. Matthew Edwards,
No information about this author
Warda Mustfa,
No information about this author
Shahaba Tehreem
No information about this author
et al.
Food and Chemical Toxicology,
Journal Year:
2024,
Volume and Issue:
190, P. 114816 - 114816
Published: June 14, 2024
Language: Английский
Alpha-Lipoic acid alleviates imidacloprid-induced neuro-behavioral deficits in rats via Nrf2/HO-1 pathway
Toxicology Mechanisms and Methods,
Journal Year:
2023,
Volume and Issue:
34(2), P. 176 - 188
Published: Oct. 30, 2023
Imidacloprid
(IMI),
a
widely
used
pesticide
in
agriculture
and
potential
food
contaminant,
poses
significant
health
concerns.
This
study
sought
to
comprehensively
evaluate
its
neurotoxic
effects
while
investigating
the
protective
role
of
alpha-lipoic
acid
(ALA),
naturally
occurring
dietary
antioxidant
renowned
for
capacity
combat
oxidative
stress,
support
cardiovascular
health,
maintain
optimal
nerve
function.
In
this
study,
28
rats
were
divided
evenly
into
four
groups
administered
oral
treatments
corn
oil,
IMI,
IMI
+
ALA,
respectively.
The
results
indicated
that
exposed
exhibited
neurobehavioral
impairments,
decreased
levels
enzymes
acetylcholinesterase
activity,
reduced
expression
HO-1
Nrf2,
increased
pro-inflammatory
cytokines
like
IL-6
TNF-α
their
hippocampal
tissues.
Furthermore,
histopathological
analysis
brain
tissues,
specifically
cortex
hippocampus,
from
IMI-treated
group
revealed
varying
degrees
neuronal
degeneration.
contrast,
co-administered
ALA
alongside
showed
noticeable
improvements
all
assessed
toxicological
parameters.
underscores
vital
significance
as
therapeutic
adjunct
mitigating
adverse
consequences
insecticide
exposure.
By
harnessing
Nrf2/HO-1
pathway,
demonstrates
ability
shield
against
IMI-induced
neurotoxicity,
offering
promising
avenue
enhancing
public
safety.
As
result,
our
findings
advocate
incorporation
daily
supplement
fortify
resilience
stress-related
deficits
linked
exposure,
thereby
advancing
understanding
neuroprotection
strategies
face
environmental
challenges.
Language: Английский
Imidacloprid unique and repeated treatment produces cholinergic transmission disruption and apoptotic cell death in SN56 cells.
Paula Moyano,
No information about this author
Andrea Flores,
No information about this author
Javier San Juan
No information about this author
et al.
Food and Chemical Toxicology,
Journal Year:
2024,
Volume and Issue:
193, P. 114988 - 114988
Published: Sept. 7, 2024
Language: Английский
Ascorbic acid supplementation in adolescent rats ameliorates anxiety‐like and depressive‐like manifestations of nicotine‐ethanol abstinence: Role of oxidative stress, inflammatory, and serotonergic mechanisms
Alireza Najafzadeh,
No information about this author
M Mahdizadeh,
No information about this author
Samaneh Kakhki
No information about this author
et al.
International Journal of Developmental Neuroscience,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Dec. 4, 2024
Abstract
Background
The
present
study
aims
to
assess
the
therapeutic
potential
of
vitamin
C
(Vit
C)
on
anxiety‐
and
depressive‐like
behavior
induced
by
abstinence
from
chronic
nicotine‐ethanol
co‐exposure
in
adolescent
male
rats.
Materials
methods
Adolescent
rats
were
divided
into
seven
experimental
groups
with
ten
as
follows:
1)
vehicle,
2)
Nicotine
(Nic)‐Ethanol
(Eth):
received
Nic
(2
mg/kg)
Eth
(20%)
drinking
water
21
42
days
age,
3–5)
Nic‐Eth‐Vit
100/200/400:
age
Vit
100/200/400
mg/kg
43
63
6)
Nic‐Eth‐Bupropion
(Bup)‐
Naloxone
(Nal):
Bup
Nal
7)
400
mg/kg:
age.
Behavioral
assessments
done
elevated
plus
maze
(EPM),
forced
swimming
test
(FST),
marble
burring
(MBT),
open
field
tests
(OFT).
Furthermore,
specific
biochemical
variables
associated
oxidative,
inflammatory,
serotonergic
profiles
quantified.
Results
According
obtained
results,
anxiety
depression
treated
We
showed
that
two
higher
doses
increases
active
struggling
time
FST
decreases
both
spent
peripheral
zone
OFT
closed
arms
EPM.
In
addition,
animals
buried
less
number
marbles
MBT
compared
their
control
counterparts.
oxidative
stress
inflammation
cortical
tissues
Biochemical
parameters
improved
Nic‐Eth
group
receiving
200/400
Bup‐Nal
through
establishing
a
balance
between
oxidant/anti‐oxidant
inflammatory/anti‐inflammatory
mediators.
serotonin
level
was
increased,
while
Monoamine
oxidase
(MAO)
activity
notably
decreased.
Conclusion
findings
support
beneficial
effect
withdrawal
various
mechanisms
such
promotion
antioxidant
defense,
suppression
inflammatory
mediators,
enhancement
serotoninergic
function.
Language: Английский