Cell Biochemistry and Function,
Год журнала:
2024,
Номер
42(8)
Опубликована: Ноя. 5, 2024
ABSTRACT
Radiation
therapy
is
indispensable
in
medical
practice
but
often
causes
adverse
effects
on
healthy
tissues,
necessitating
the
search
for
natural
radioprotectors.
This
study
investigates
protective
effect
of
Biochanin
A
(BCA)
against
gamma
radiation‐induced
oxidative
stress
and
DNA
damage
Swiss
albino
mice.
Gamma
radiation,
a
potent
ionizing
source,
generates
reactive
oxygen
species
(ROS)
that
cellular
biomolecules,
including
DNA.
Antioxidants
play
crucial
role
neutralizing
ROS
preventing
damage.
mice
were
divided
into
control,
BCA
control
(10
mg/kg
body
weight),
radiation
alone
(7
Gy),
radiation+
pretreatment
groups.
BCA,
isoflavone
with
known
antioxidant
cytoprotective
properties,
was
administered
intraperitoneally
before
exposure.
After
irradiation,
lipid
peroxidation
levels,
enzyme
activities/level
(superoxide
dismutase,
catalase,
glutathione
peroxidase
reduced
glutathione),
expression
levels
repair
genes
(P53,
P21,
GADD45α),
apoptotic
markers
(Bax,
Bcl‐2,
Caspase‐3,
‐9
Cytochrome‐C),
inflammatory
marker
(NF‐κB)
analyzed
small
intestine
tissue.
Our
findings
indicate
significantly
elevated
altered
activities,
indicating
stress.
However,
mitigated
these
by
bolstering
defences,
reducing
Additionally,
markers,
NF‐κB
expression,
promoting
cell
survival
mechanisms.
At
molecular
level,
upregulated
key
repairing
maintaining
genomic
stability.
These
results
underscore
potential
as
radioprotector,
suggesting
its
efficacy
mitigating
preserving
integrity.
In
conclusion,
demonstrates
promising
radioprotective
properties
attenuating
stress,
enhancing
modulating
pathways,
mechanisms
following
Further
research
necessary
to
elucidate
precise
action
explore
therapeutic
applications
oncology
environmental
radioprotection.
Cell Biochemistry and Biophysics,
Год журнала:
2025,
Номер
unknown
Опубликована: Фев. 19, 2025
Abstract
Idiopathic
Pulmonary
Fibrosis
(IPF)
is
a
severe,
rapidly
advancing
disease
that
drastically
diminishes
life
expectancy.
Without
treatment,
it
can
progress
to
lung
cancer.
The
precise
etiology
of
IPF
remains
unknown,
but
inflammation
and
damage
the
alveolar
epithelium
are
widely
thought
be
pivotal
in
its
development.
Research
has
indicated
activating
NLRP3
inflammasome
crucial
mechanism
pathogenesis,
as
triggers
release
pro-inflammatory
cytokines
such
IL-1β,
IL-18,
TGF-β.
These
contribute
myofibroblast
differentiation
extracellular
matrix
(ECM)
accumulation.
Currently,
treatment
options
for
limited.
Only
two
FDA-approved
medications,
pirfenidone
nintedanib,
available.
While
these
drugs
decelerate
progression,
they
come
with
range
side
effects
do
not
cure
disease.
Additional
strategies
primarily
involve
supportive
care
therapy.
Emerging
research
highlighted
numerous
flavonoids
derived
from
traditional
medicines
inhibit
critical
regulators
responsible
inflammasome.
show
promise
potential
therapeutic
agents
managing
IPF,
offering
new
avenue
targets
core
inflammatory
processes
this
debilitating
condition.
Graphical
Ecotoxicology and Environmental Safety,
Год журнала:
2024,
Номер
281, С. 116661 - 116661
Опубликована: Июль 1, 2024
Baicalin
has
antioxidative,
antiviral,
and
anti-inflammatory
properties.
However,
its
ability
to
alleviate
oxidative
stress
(OS)
DNA
damage
in
liver
cells
exposed
aflatoxin
B1
(AFB1),
a
highly
hepatotoxic
compound,
remains
uncertain.
In
this
study,
the
protective
effects
of
baicalin
on
AFB1-induced
hepatocyte
injury
mechanisms
underlying
those
were
investigated.
Stable
cell
lines
expressing
CYP3A4
established
using
lentiviral
vectors
assess
levels
by
conducting
assays
determine
content
reactive
oxygen
species
(ROS),
malondialdehyde
(MDA),
superoxide
dismutase
(SOD).
Additionally,
was
evaluated
8-hydroxy-2-deoxyguanosine
(8-OHdG)
comet
assays.
Transcriptome
sequencing,
molecular
docking,
vitro
experiments
conducted
injury.
vivo,
rat
model
induced
AFB1
used
evaluate
baicalin.
vitro,
significantly
attenuated
caused
due
OS,
as
determined
decrease
ROS,
MDA,
SOD
levels.
also
considerably
decreased
hepatocytes.
This
effect
found
be
closely
associated
with
TP53-mediated
ferroptosis
pathway.
To
elaborate,
physically
interacts
P53,
leading
suppression
expression
GPX4
SLC7A11,
which
turn
inhibits
ferroptosis.
vivo
findings
showed
that
AFB1-treated
tissues,
γ-H2AX
an
increase
SLC7A11
Overexpression
TP53
weakened
can
OS
via
theoretical
foundation
for
use
protecting
from
toxic
AFB1.
BMC Complementary Medicine and Therapies,
Год журнала:
2024,
Номер
24(1)
Опубликована: Янв. 9, 2024
Abstract
Background
Legg-Calvé-Perthes
disease
is
a
special
self-limited
in
pediatric
orthopedics
with
high
disability
rate
and
long-term
course,
there
still
no
clear
effective
therapeutic
drug
clinic.
This
study
aimed
to
investigate
the
potential
efficacy
of
biochanin
A,
kind
oxygen-methylated
isoflavone
compound,
treating
Perthes
based
on
network
pharmacology,
molecular
docking
vitro
experiments.
Methods
IL-6
was
used
stimulate
human
umbilical
vein
endothelial
cells
construct
cell
dysfunction
model.
We
demonstrated
whether
A
could
alleviate
through
CCK8
assay,
immunofluorescence.
Targets
from
pharmMappeer,
SWISS,
TargetNet
databases
were
screened.
obtained
Genecards
OMIM
databases.
Protein–protein
interaction,
Gene
Ontology,
Kyoto
Encyclopedia
Genes
Genomics
analyses
analyze
target
key
pathway
anti-endothelial
activity
A.
To
validate
target-drug
interactions,
dynamics
simulations
performed
result
proved
by
western
blot.
Results
It
found
that
can
promote
expression
ZO-1,
reduce
ICAM-1,
which
means
improving
dysfunction.
total
585
targets
10,832
527
overlapping
obtained.
AKT1,
TNF-α,
VCAM1,
ICAM1,
NOS3
might
be
pathways
PI3K-Akt
TNF
signaling
pathways.
Molecular
results
indicated
AKT1
TNF-α
had
highest
affinity
binding
Conclusion
indicates
induced
disease,
provides
theoretical
basis
for
treatment
using
Reproductive Biology and Endocrinology,
Год журнала:
2025,
Номер
23(1)
Опубликована: Янв. 25, 2025
Endocrine-disrupting
chemicals
(EDCs)
interfere
with
the
endocrine
system
and
negatively
impact
reproductive
health.
Biochanin
A
(BCA),
an
isoflavone
anti-inflammatory
estrogen-like
properties,
has
been
identified
as
one
such
EDC.
This
study
investigates
effects
of
BCA
on
transcription,
metabolism,
hormone
regulation
in
primary
human
granulosa
cells
(GCs),
a
specific
focus
activation
bitter
taste
receptors
(TAS2Rs).
Primary
GCs
from
60
participants
were
treated
10
µM
BCA,
selective
antagonists
used
to
block
TAS2R
activation.
The
assessed
expression
TAS2R14
TAS2R43,
analyzed
StAR
CYP17A1
gene
expression.
Intracellular
calcium
levels,
lipid
droplet
size,
mitochondrial
network
complexity
measured
evaluate
cellular
metabolism
energy
dynamics.
treatment
significantly
upregulated
TAS2R43
expression,
leading
70%
increase
mRNA
levels
twofold
(p
<
0.05).
These
reversed
by
antagonists.
Additionally,
decreased
intracellular
Ca2+
0.01)
reduced
size
0.001),
both
which
counteracted
Enhanced
0.001)
was
also
observed,
suggesting
increased
fusion
improved
findings
indicate
that
modulates
transcriptional
metabolic
processes
through
TAS2Rs,
highlighting
their
role
regulation.
statistically
significant
results
emphasize
relevance
further
exploring
EDCs
like
Collaborative
research
efforts
are
essential
address
mitigate
adverse
impacts
fertility.
