Drug and Chemical Toxicology,
Journal Year:
2021,
Volume and Issue:
46(1), P. 97 - 103
Published: Dec. 9, 2021
The
aim
of
the
present
study
was
to
evaluate
protective
effect
gallic
acid
(GA)
against
cisplatin
(CDDP)-induced
ovarian
toxicity,
for
first
time.
damage
generated
with
CDDP
(5
mg/kg)
intraperitoneally
(i.p.)
administration
in
rats.
GA
(2.5
and
5
were
administered
i.p.
3
consecutive
days.
carried
out
main
groups
containing
6
rats
each
group:
control,
mg/kg),
CDDP,
+
mg/kg).
levels
malondialdehyde
(MDA),
total
oxidant
status
(TOS),
antioxidant
(TAS),
oxidative
stress
index
(OSI),
catalase
(CAT),
8-hydroxy-2'-deoxyguanosine
(8-OHdG),
caspase-3
tumor
necrosis
factor-alpha
(TNF-α)
determined.
Hematoxylin
eosin
staining
method
employed
histopathological
examination.
In
group,
it
is
determined
that
statistically
significant
decreasing
TAS
CAT,
increasing
MDA,
TOS,
OSI,
8-OHdG,
TNF-α
(p
<
0.05)
compared
control
group.
administrations
significantly
restored
this
0.05).
Although
vascular
congestion,
edema,
hemorrhage,
follicular
degeneration
leukocyte
infiltration
higher
group
than
these
damages
conclusion,
showed
prevented
CDDP-induced
its
antioxidant,
anti-apoptotic
anti-inflammatory
activities.
More
comprehensive
studies
are
needed
see
underlying
mechanisms.
Frontiers in Molecular Biosciences,
Journal Year:
2019,
Volume and Issue:
6
Published: Oct. 18, 2019
Various
internal
and
external
factors
negatively
affect
the
homeostatic
equilibrium
of
organisms
at
molecular
to
whole-body
level,
inducing
so-called
state
'stress'.
Stress
affects
an
organism's
welfare
status
induces
energy-consuming
mechanisms
combat
subsequent
ill
effects;
thus,
individual
may
be
immunocompromised,
making
them
vulnerable
pathogens.
The
information
presented
here
has
been
extensively
reviewed,
compiled
analyzed
from
authenticated
published
resources
available
on
Medline,
Pubmed,
Pubmed
Central,
Science
Direct,
other
scientific
databases.
levels
can
monitored
by
quantitative
qualitative
measurement
biomarkers.
Prominent
markers
stress
include
thermal
like
heat
shock
proteins
(HSPs),
innate
immune
Acute
Phase
Proteins
(APPs),
oxidative
markers,
chemical
secretions
in
saliva
urine.
In
addition,
biomarkers
are
thought
play
critical
roles
prognosis
stress-related
diseases
disorders,
therapy
guidance.
Moreover,
different
components
have
identified
as
potent
mediators
cardiovascular,
central
nervous
system,
hepatic,
nephrological
which
also
employed
evaluate
these
conditions
precisely,
but
with
stringent
validation
specificity.
Considerable
advances
made
detection,
quantitation,
application
present
review
describes
current
progress
identifying
biomarkers,
their
prognostic
therapeutic
values.
International Journal of Molecular Sciences,
Journal Year:
2019,
Volume and Issue:
20(4), P. 874 - 874
Published: Feb. 18, 2019
The
latest
studies
have
indicated
a
strong
relationship
between
systemic
insulin
resistance
(IR)
and
higher
incidence
of
neurodegeneration,
dementia,
mild
cognitive
impairment.
Although
some
these
abnormalities
could
be
explained
by
chronic
hyperglycaemia,
hyperinsulinemia,
dyslipidaemia,
and/or
prolonged
whole-body
inflammation,
the
key
role
is
attributed
to
neuronal
redox
imbalance
oxidative
damage.
In
this
mini
review,
we
provide
schematic
overview
intracellular
stress
mitochondrial
in
IR
brain.
We
highlight
important
correlations
found
so
far
brain
stress,
ceramide
generation,
β-amyloid
accumulation,
as
well
apoptosis
conditions.
International Journal of Molecular Sciences,
Journal Year:
2022,
Volume and Issue:
23(5), P. 2687 - 2687
Published: Feb. 28, 2022
Globally,
the
incidence
of
type
2
diabetes
mellitus
(T2DM)
and
Alzheimer’s
disease
(AD)
epidemics
is
increasing
rapidly
has
huge
financial
emotional
costs.
The
purpose
current
review
article
to
discuss
shared
pathophysiological
connections
between
AD
T2DM.
Research
findings
are
presented
underline
vital
role
that
insulin
plays
in
brain’s
neurotransmitters,
homeostasis
energy,
as
well
memory
capacity.
this
indicate
existence
a
mechanistic
interplay
pathogenesis
with
T2DM
and,
especially,
disrupted
signaling.
interlinked
resistance,
neuroinflammation,
oxidative
stress,
advanced
glycosylation
end
products
(AGEs),
mitochondrial
dysfunction
metabolic
syndrome.
Beta-amyloid,
tau
protein
amylin
can
accumulate
brains.
Given
patients
not
routinely
evaluated
terms
their
cognitive
status,
they
rarely
treated
for
impairment.
Similarly,
high
levels
or
Studies
suggesting
caused
by
resistance
brain
also
offer
strong
support
hypothesis
3
diabetes.
Molecular Metabolism,
Journal Year:
2021,
Volume and Issue:
52, P. 101234 - 101234
Published: April 16, 2021
The
brain
was
once
thought
of
as
an
insulin-insensitive
organ.
We
now
know
that
the
insulin
receptor
is
present
throughout
and
serves
important
functions
in
whole-body
metabolism
function.
Brain
signaling
involved
not
only
homeostatic
processes
but
also
neuropathological
such
cognitive
decline
Alzheimer's
disease.
Biomedicine & Pharmacotherapy,
Journal Year:
2018,
Volume and Issue:
111, P. 503 - 516
Published: Dec. 28, 2018
Obesity
and
overweight
have
increased
at
an
alarming
rate
in
the
world
during
last
three
decades.
is
a
crucial
factor
development
of
metabolic
abnormalities,
including
glucose
intolerance,
insulin
resistance,
syndrome,
low-grade
inflammation
oxidative
stress.
A
similar
scinario
occurs
aging
process
where
alterations
energetic
metabolism
homeostasis
chronic
systematic
been
observed.
Oxidative
stress
poor
physical
performance
can
increase
risk
disease.
Despite
diverse
studies
on
pathophysiological
effects
obesity,
its
impact
related
to
gender
through
life,
particularly
aging,
hasn’t
received
reasonable
attention.
The
purpose
this
review
outline
mechanisms
associated
with
emphasis
monosodium
glutamate
(MSG)-induced
obese
model.
MSG-induced
obesity
declined
adiponectin
were
more
obvious
male
mice,
while
tolerance,
sensitivity
redox
balance
altered
age
both
female
mice.
These
findings
indicate
that
are
as
well
aging.
Therefore,
MSG
model
resonable
value
underlie
relationship
between
gender,
obesity.
In
addition,
we
reviewed
medicinal
plants
their
active
constituents
which
used
treat
Given
significat
model,
needed
scrutinize
benificial
underlying
proven
anti-obesity
activity.
Frontiers in Neuroscience,
Journal Year:
2019,
Volume and Issue:
12
Published: Jan. 8, 2019
Metabolic
syndrome
and
diabetes
impact
brain
function
metabolism.
While
it
is
well
established
that
rodents
exposed
to
diets
rich
in
saturated
fat
develop
dysfunction,
contrasting
results
abound
the
literature,
likely
as
result
of
exposure
different
high-fat
diet
(HFD)
compositions
for
varied
periods
time.
In
present
study,
we
investigated
alterations
hippocampal-dependent
spatial
memory
by
measuring
Y-maze
spontaneous
alternation,
metabolic
profiles
hippocampus,
cortex
hypothalamus
1H
magnetic
resonance
spectroscopy
(MRS),
levels
proteins
specific
synaptic
glial
compartments
mice
6
months
amounts
(10,
45,
or
60%
total
energy
intake).
Increasing
dietary
amount
from
10
45%
resulted
obesity
accompanied
increased
leptin,
fasting
blood
glucose
insulin,
reduced
tolerance.
comparison
controls
(10%-fat),
only
fed
60%-fat
showed
glycemia,
plasma
corticosterone
has
a
major
on
function.
HFD-induced
profile
modifications
measured
MRS
were
observed
across
three
areas
60%-
but
not
45%-fat
diet,
while
both
HFD
groups
displayed
impaired
memory.
also
affected
systems
involved
neuro-
gliotransmission
hippocampus.
Namely,
relative
controls,
60%-fat-fed
SNAP-25,
PSD-95
syntaxin-4
immunoreactivity,
45%-fat-fed
gephyrin
immunoreactivity.
For
levels,
reductions
vesicular
glutamate
transporter
vGlut1
GABA
hippocampus
hypothalamus,
controls.
Immunoreactivity
against
GFAP
and/or
Iba-1
was
higher
than
suggesting
occurrence
gliosis.
We
conclude
distinct
neurochemical
brain.
Journal of Clinical Medicine,
Journal Year:
2019,
Volume and Issue:
8(11), P. 1815 - 1815
Published: Nov. 1, 2019
The
study
aims
to
explore
the
oxidative
status
related
inflammation
in
peripheral
blood
of
stable
relapsing-remitting
multiple
sclerosis
(MS)
patients
with
low
disability.
In
this
study,
31
people
were
included
and
divided
into
two
groups:
an
MS
group
which
16
a
disability
level
(age
38.9
±
7.08,
EDSS
median
2.5)
control
that
contains
15
healthy
volunteers
similar
age
group.
Thiobarbituric
acid
reactive
substances
(TBARS),
protein
carbonyl
(PCO),
total
antioxidant
capacity
(TAC)
as
stress
markers,
neutrophil/lymphocyte
ratio
(NLR),
erythrocyte
sedimentation
rate
(ESR)
analyzed
sample
establish
stress/inflammatory
using
conventional
plasma
markers.
we
showed
pro-inflammatory
relapse-remitting
stage
diseases
can
be
easily
accurately
appreciated
by
NLR.
An
increased
NLR
is
associated
decreased
capacity,
even
early
neuronal
damage.
Oxidative
aggravates
functional
outcome,
potentiates
damage,
accelerate
progression
disease.
International Journal of Molecular Sciences,
Journal Year:
2022,
Volume and Issue:
23(5), P. 2577 - 2577
Published: Feb. 25, 2022
One
of
the
most
common
lipids
in
human
body
is
palmitic
acid
(PA),
a
saturated
fatty
with
essential
functions
brain
cells.
PA
used
by
cells
as
an
energy
source,
besides
being
precursor
signaling
molecules
and
protein
tilting
across
membrane.
Although
plays
physiological
brain,
its
excessive
accumulation
leads
to
detrimental
effects
on
cells,
causing
lipotoxicity.
This
mechanism
involves
activation
toll-like
receptors
(TLR)
nuclear
factor
kappa-light-chain-enhancer
activated
B
(NF-κB)
pathways,
consequent
release
pro-inflammatory
cytokines,
increased
production
reactive
oxygen
species
(ROS),
endoplasmic
reticulum
(ER)
stress,
autophagy
impairment.
Importantly,
some
cellular
changes
induced
lead
augmented
susceptibility
development
Alzheimer’s
Parkinson´s
diseases.
Considering
complexity
response
intrinsic
differences
this
review,
we
provide
overview
molecular
different
their
possible
relationships
neurodegenerative
diseases
(NDs).
Furthermore,
propose
use
other
acids,
such
oleic
or
linoleic
acid,
potential
therapeutic
approaches
against
NDs,
these
acids
can
counteract
PA’s
negative
Current Opinion in Neurobiology,
Journal Year:
2023,
Volume and Issue:
79, P. 102694 - 102694
Published: Feb. 24, 2023
Type
2
diabetes
(T2D)
and
Alzheimer's
disease
(AD)
are
two
global
epidemics
that
share
several
metabolic
defects,
such
as
insulin
resistance,
impaired
glucose
metabolism,
mitochondrial
defects.
Importantly,
strong
evidence
demonstrates
T2D
significantly
increases
the
risk
of
cognitive
decline
dementia,
particularly
AD.
Here,
we
provide
an
overview
defects
characterize
link
both
pathologies
putting
focus
on
mitochondria.
The
biomarker
potential
components
therapeutic
some
drugs
target
modulate
mitochondria
also
briefly
discussed.