Abstract
Background
Oligoasthenozoospermia
is
a
common
cause
of
male
infertility,
for
which
effective
treatments
are
urgently
needed.
Humanin
(HN)
peptide
associated
with
this
condition.
Objectives
To
investigate
the
ameliorative
effect
[Gly14]‐Humanin
(HNG)
on
oligoasthenozoospermia
and
mechanisms.
Materials
methods
Mice
were
treated
cyclophosphamide
(CP)
to
construct
mice
model
oligoasthenozoospermia.
The
resulting
saline
or
HNG.
Subsequently,
testis
weights,
organ
indices,
testicular
structure,
sperm
counts
motilities,
litter
sizes,
serum
testosterone
concentrations
determined.
Differential
gene
expression
in
tissues
was
determined
by
RNA
sequencing.
TM3,
TM4,
GC1,
GC2
cells
exposed
erastin
induce
ferroptosis,
followed
treatment
HNG
+
ML385
(a
nuclear
factor
erythroid
2‐related
2
inhibitor).
Levels
reactive
oxygen
species
(ROS),
malondialdehyde
(MDA),
glutathione
(GSH),
ferrous
ions
(Fe
2+
)
their
ferroptosis‐related
proteins
immunofluorescence
western
blot.
Results
improved
parameters
increased
size
mice.
Kyoto
Encyclopaedia
Genes
Genomes
pathway
enrichment
analysis
revealed
significant
differential
genes.
after
treatment.
ROS,
MDA,
Fe
decreased
GSH
TM3
TM4
In
vitro
experiments
confirmed
that
activated
2/glutathione
peroxidase
4
(Nrf2/GPX4)
pathway.
However,
these
effects
blocked
Discussion
conclusion
demonstrated
therapeutic
mouse
reducing
oxidative
stress
ferroptosis.
cells,
attenuated
cellular
inhibited
ferroptosis
via
Nrf2/GPX4
Phytotherapy Research,
Год журнала:
2024,
Номер
38(11), С. 5203 - 5224
Опубликована: Авг. 27, 2024
Abstract
Glucocorticoid‐induced
osteoporosis
(GIOP)
commonly
accelerates
bone
loss,
increasing
the
risk
of
fractures
and
osteonecrosis
more
significantly
than
traditional
menopausal
osteoporosis.
The
extracellular
environment
influenced
by
glucocorticoids
heightens
fracture
risks.
Fraxin
(Fra),
a
key
component
Chinese
herbal
remedy
Cortex
Fraxini
,
is
known
for
its
wide‐ranging
pharmacological
effects,
but
impact
on
GIOP
remains
unexplored.
This
investigation
aims
to
delineate
effects
underlying
mechanisms
Fra
in
combating
dexamethasone
(Dex)‐induced
ferroptosis
GIOP.
We
established
mouse
model
via
intraperitoneal
injections
Dex
cultured
osteoblasts
with
treatment
vitro
analysis.
evaluated
Dex‐treated
through
assays
such
as
C11‐BODIPY
FerroOrange
staining,
mitochondrial
functionality
tests,
protein
expression
analyses
Western
blot
immunofluorescence.
influence
microarchitecture
mice
was
assessed
using
microcomputerized
tomography,
hematoxylin
eosin
double‐labeling
Calcein–Alizarin
Red
S,
immunohistochemistry
at
imaging
histological
levels.
Based
our
data,
prevented
Dex‐induced
loss.
In
vitro,
glutathione
levels
increased
malondialdehyde,
lipid
peroxidation,
reactive
oxygen
species
decreased.
also
increases
nuclear
factor
erythroid
2‐related
2
(Nrf2),
peroxidase
4
(GPX4),
COL1A1
promotes
formation.
To
delve
deeper
into
mechanism,
findings
revealed
that
triggered
activation
Nrf2/GPX4
signaling.
Moreover,
use
siRNA‐Nrf2
blocked
beneficial
effect
cultivated
Dex.
effectively
combats
activating
signaling
pathway
inhibit
ferroptosis.
Journal of Nanobiotechnology,
Год журнала:
2025,
Номер
23(1)
Опубликована: Март 29, 2025
Heart
failure
(HF)
is
a
prevalent
and
critical
cardiac
condition
that
leads
to
profound
structural
functional
changes
in
the
heart.
Although
traditional
treatments
have
shown
partial
efficacy,
long-term
outcomes
remain
suboptimal.
Emerging
research
has
highlighted
pivotal
role
of
oxidative
stress
ferroptosis
HF
progression.
This
study
investigates
new
therapeutic
approach
utilizing
antioxidant
polyphenol
nanoparticles
loaded
with
STAT3
agonist
(PN@Col)
target
these
pathways
improve
age-related
HF.
Key
cells
genes
contributing
progression
were
identified
via
analysis
GEO
database,
single-cell
RNA
sequencing
(scRNA-seq)
AUCell
used
evaluate
differential
gene
expression.
The
was
as
essential,
its
functionality
further
validated
vitro
through
cell
experiments,
confirming
impact
on
cardiomyocytes
(CMs)
Following
development
PN@Col,
experiments
showed
PN@Col
effectively
reduced
CMs.
In
vivo
studies
elderly
mice
demonstrated
significant
improvements
function
following
treatment.
offers
promising
by
mitigating
cardiomyocytes.
These
findings
provide
solid
scientific
foundation
for
potential
novel
treatment
strategy
HF,
supporting
exploration
toward
clinical
application.
Pharmacological Research,
Год журнала:
2024,
Номер
206, С. 107268 - 107268
Опубликована: Июнь 20, 2024
Heart
failure
(HF)
has
emerged
as
the
most
pressing
health
concerns
globally,
and
extant
clinical
therapies
are
accompanied
by
side
effects
patients
have
a
high
burden
of
financial.
The
protein
products
nuclear
factor
erythroid
2-related
2
(Nrf2)
target
genes
variety
cardioprotective
effects,
including
antioxidant,
metabolic
functions
anti-inflammatory.
By
evaluating
established
preclinical
research
in
HF
to
date,
we
explored
potential
Nrf2
exert
unique
novel
therapeutic
receptor
for
HF.
In
this
review,
generalize
progression,
structure,
function
cardiovascular
system.
mechanism
action
involved
well
agonists
natural
compounds
summarized.
Additionally,
discuss
challenges
implications
future
translation
application
pharmacology
targeting
Nrf2.
It's
critical
developing
new
drugs
Biomolecules,
Год журнала:
2024,
Номер
14(9), С. 1142 - 1142
Опубликована: Сен. 9, 2024
Nasopharyngeal
carcinoma
(NPC)
is
closely
linked
to
Epstein–Barr
virus
(EBV)
infection.
Curcumae
Rhizoma,
a
traditional
Chinese
herb,
has
shown
antitumor
effects,
primarily
through
its
component
curcumol
(Cur),
which
been
reduce
NPC
cell
invasion
and
migration
by
targeting
nucleolin
(NCL)
Virus
Nuclear
Antigen
1
(EBNA1).
We
constructed
an
EBV-positive
model
using
C666-1
cells
performed
transcriptomics
studies
after
treatment
with
curcumol,
revealed
significant
enrichment
of
ubiquitin-mediated
proteolysis,
the
PI3K-AKT
mTOR
signaling
pathways,
cycle
apoptosis
involved
in
tumor
migration.
To
investigate
importance
NCL
EBNA1
curcumol-resistant
NPC,
we
multi-omics
study
short
hairpin
(shNCL)
shEBNA1
cells,
proteomics
results
showed
complement
coagulation
cascades
proteolysis
pathways.
Here,
focused
on
ubiquitin-conjugating
enzyme
E2C
(UBE2C),
plays
important
role
pathway.
In
addition,
metabolomics
that
UBE2C
highly
associated
4-Aminobutanoic
acid
(GABA).
vitro
further
validated
function
key
targets,
suggesting
EBNA1-mediated
resistance
nasopharyngeal
metastasis.