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
Natural Product Communications,
Год журнала:
2024,
Номер
19(10)
Опубликована: Окт. 1, 2024
Objective:
To
explore
the
ameliorative
effect
and
mechanism
of
action
sericin
on
liver
injury
in
Non-Alcoholic
Fatty
Liver
Disease
(NAFLD)
model
mice.
Methods:
Mice
were
fed
a
high-fat
diet
for
8
weeks
to
establish
NAFLD
The
mice
then
randomly
divided
into
6
groups
given
0,
250,
500,
1000
mg/kg
body
weight
sericin,
+
ML385
(a
protein
inhibitor
Nrf2),
Zhibitai
Capsules
positive
drug),
by
gavage,
respectively.
levels
TC,
TG,
low-density
lipoprotein
cholesterol
(LDL-C),
high-density
(HDL-C),
alanine
aminotransferase
(ALT),
aspartate
(AST)
mouse
serum
MDA,
GSH,
SOD,
TNF-α,
IL-6
tissues
measured.
Pathological
changes
evaluated
using
hematoxylin-eosin
(HE)
Oil
Red
O
staining.
Protein
expression
Nrf2,
Keap1,
HO-1,
GPX4,
NF-κB
p65
was
detected
Western
blotting,
level
GPX4
examined
immunohistochemistry.
Results:
Sericin
improved
hepatic
steatosis
lipid
accumulation
LDL-C,
down-regulated,
HDL-C
SOD
up-regulated.
There
no
significant
difference
AST
ALT
all
groups.
In
addition,
upregulated
keap1,
proteins
inhibited
lipids
indices
between
group
dose
Conclusion:
has
an
alleviating
oxidative
stress
inflammatory
responses
injury.
It
remains
be
explored
whether
this
is
regulated
through
Nrf2-
GPX4/
signaling
pathway.
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
