bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2022,
Volume and Issue:
unknown
Published: Oct. 4, 2022
Abstract
Cystic
echinococcosis
(CE)
is
one
of
the
most
widespread
and
harmful
zoonotic
parasitic
diseases
it
commonly
affects
liver.
In
this
study,
we
characterized
multiple
changes
in
mouse
hepatocytes
following
treatment
with
excretory-secretory
(ES)
products
Echinococcus
granulosus
protoscoleces
by
a
factorial
experiment.
The
cell
counting
kit-8
assay
(CCK-8),
5-ethynyl-2’-deoxyuridine
(EdU)
assay,
flow
cytometry
were
used
to
detect
growth
hepatocytes.
Inverted
microscopy,
scanning
electron
microscopy
(SEM),
transmission
(TEM)
observe
morphology
ultrastructure
An
automatic
biochemical
analyzer
an
ELISA
detection
kit
determine
six
conventional
hepatocyte
enzymatic
indices,
levels
five
hepatocyte-synthesized
substances,
contents
glucose
lactate.
Western
blot
analysis
was
conducted
analyze
protein
expression
rate-limiting
enzymes
metabolism
pathway
hepatocytes:
glutamic-pyruvic
transaminase
(ALT),
glutamic-oxalacetic
(AST),
alkaline
phosphatase
(ALP),
lactate
dehydrogenase
(LDH),
gamma-glutamyl
transpeptidase
(GGT),
leucine
arylamidase
(LAP).
results
CCK-8
EdU
assays
both
showed
that
ES
could
inhibit
proliferation
hepatocytes,
indicated
promote
apoptosis
After
treatment,
disrupted
certain
extent.
membrane
microvilli
observed
through
SEM,
nucleus,
mitochondria,
rough
endoplasmic
reticulum
TEM.
activities
increased
addition
Fe
synthesis
albumin
(ALB),
uric
acid
(UA),
urea,
whereas
transferrin
(TRF)
decreased.
all
key
decreased,
biological
effects
significantly
inhibited.
We
analyzed
causes
possible
complications
caused
various
advocate
corresponding
measures.
also
propose
mechanisms
which
cause
necrosis,
but
specific
mechanism
requires
further
study.
Author
Summary
,
widely
distributed
infected
tapeworm,
has
serious
economic
social
burdens
pastoral
areas
China.
metacestodes
mainly
infect
liver
intermediate
hosts
(humans,
cattle,
sheep,
etc.).
Currently,
on
hepatocytes’
ultrastructure,
enzymology,
function,
have
not
been
characterized,
accurate
characterization
crucial
study
related
pathogenesis
preventive
therapy.
Here,
characterize
using
action
found
inhibited
promoted
apoptosis.
can
degree
damage
membrane,
indexes
elevated,
they
ALT,
AST,
LDH,
ALP,
GGT,
LAP,
Fe,
ALB,
UA,
urea
synthesized
higher
TRF
lower.
Reduced
pathways
including
PFK-1,
IDH,
G-6-PD,
GS,
GP,
GLUT-2,
indicating
inhibits
Our
only
detail
proposed
causing
these
effects,
provided
basis
for
subsequent
studies
prevention,
treatment.
Research Square (Research Square),
Journal Year:
2025,
Volume and Issue:
unknown
Published: March 31, 2025
Abstract
Spinal
cord
injury
(SCI)
is
one
of
the
most
devastating
and
catastrophic
types
injury,
with
high
rates
mortality
disability.
Ferroptosis
has
become
target
many
major
incurable
human
diseases.
By
inhibiting
ferroptosis,
melatonin
(MT)
can
reduce
damage
in
various
organs,
but
protective
effect
MT
on
SCI
not
been
reported
yet.
The
modified
Ellen's
method
was
used
to
establish
an
rat
model.
spinal
neurons
recovery
motor
function
were
observed.
In
vitro
experiments,
oxygen-glucose
deprivation/reoxygenation
(OGD/R)
model
established
by
using
mouse
hippocampal
neuron
(HT22)
cells
simulate
ischemia-reperfusion
injury.
A
ferroptosis
directly
induced
Erastin
also
used.
nuclear
factor
erythroid
2-related
2
(Nrf2)
inhibitor
ML
385
further
detect
mechanism
through
which
inhibits
protects
neuronal
cells.
Our
study
demonstrates
that
rats,
promote
behavior
injured
tissue
after
SCI.
Under
electron
microscope,
inhibited
rescued
damaged
mitochondria,
partially
restored
mitochondrial
structure.
ML385,
Nrf2
inhibitor,
reversed
effects
MT.
Overall,
may
alleviate
early
activating
Nrf2/heme
oxygenase-1(HO-1)/glutathione
peroxidase
4
(GPX
4)
pathway.
World Journal of Gastroenterology,
Journal Year:
2025,
Volume and Issue:
31(15)
Published: April 17, 2025
Transjugular
intrahepatic
portosystemic
shunts
(TIPSs)
are
generally
used
for
the
management
of
complications
portal
hypertension
in
patients
with
decompensated
cirrhosis.
However,
hepatic
encephalopathy
(HE),
which
impairs
neuropsychiatric
function
and
motor
control,
remains
primary
adverse
effect
TIPS,
limiting
its
utility.
Prompt
prevention
treatment
post-TIPS
HE
critical,
as
they
strongly
associated
readmission
rates
poor
quality
life.
This
review
focuses
on
main
pathophysiological
mechanisms
underlying
HE,
explores
advanced
biomarkers
predictive
tools,
discusses
current
strategies
future
directions
to
prevent
or
reverse
following
TIPS.
These
include
preoperative
patient
assessment,
individualized
shunt
diameter
optimization,
spontaneous
embolization
during
TIPS
procedure,
postoperative
preventive
therapeutic
measures
such
nutrition
management,
medical
therapy,
fecal
microbiota
transplantation,
stent
reduction.