JHEP Reports,
Год журнала:
2023,
Номер
6(1), С. 100918 - 100918
Опубликована: Сен. 30, 2023
Current
therapies
for
the
treatment
of
alcohol-related
liver
disease
(ALD)
have
proven
largely
ineffective.
Patients
relapse
and
progresses
even
after
transplantation.
Altered
epigenetic
mechanisms
are
characteristic
alcohol
metabolism
given
excessive
acetate
NAD
depletion
play
an
important
role
in
injury.
In
this
regard,
novel
therapeutic
approaches
based
on
modulators
increasingly
proposed.
MicroRNAs,
acting
at
post-transcriptional
level,
appear
to
be
promising
new
targets
ALD.
Heliyon,
Год журнала:
2024,
Номер
10(11), С. e31195 - e31195
Опубликована: Май 16, 2024
Penthorum
chinense
Pursh
(P.
chinense),
a
functional
food,
has
been
applied
to
protect
the
liver
against
alcohol-related
fatty
disease
(ALD)
for
long
history
in
China.
This
study
was
designed
evaluate
ameliorative
activity
of
polyphenolic
fraction
P.
(PGF)
depending
on
relief
ALD.
The
ALD
mouse
model
established
by
exposing
mice
Lieber-DeCarli
alcohol
liquid
diet.
We
found
that
PGF
administration
significantly
ameliorated
alcohol-induced
injury,
steatosis,
oxidative
stress,
and
inflammation
mice.
Furthermore,
Alcohol-increased
levels
critical
hepatic
lipid
synthesis
proteins
sterol
regulatory
element
binding
transcription
factor
(SREBP-1)
diacylglycerol
o-acyltransferase
2
(DGAT2)
were
attenuated
PGF.
Similarly,
inhibited
expression
transport
protein
very
low-density
lipoprotein
receptor
(VLDLR).
Interestingly,
restored
alcohol-inhibited
carnitine
palmitoyltransferase
1
(CPT1)
peroxisome
proliferator-activated
alpha
(PPARα),
essential
acid
β-oxidation
proteins.
Mechanistic
studies
revealed
protects
hepatocyte
injury
deposition
via
SIRT1/AMPK
signaling
pathway.
In
sum,
this
research
clearly
demonstrated
protective
effects
ALD,
which
mediated
activating
pathways
hepatocytes.
provide
new
theoretical
basis
using
as
food
Alcoholism Clinical and Experimental Research,
Год журнала:
2022,
Номер
46(6), С. 928 - 940
Опубликована: Апрель 11, 2022
Hepatic
steatosis
is
an
early
pathology
of
alcohol-associated
liver
disease
(ALD).
Fatty
acid-binding
protein-4
(FABP4,
a
FABP
not
normally
produced
in
the
liver)
secreted
by
hepatocytes
ALD
and
stimulates
hepatoma
proliferation
migration.
This
study
sought
to
investigate
mechanism[s]
which
hepatic
ethanol
metabolism
regulates
FABP4
steatosis.Human
cells
(HepG2/HuH7)
stably
transfected
express
cytochrome
P450
2E1
(CYP2E1),
were
exposed
absence
or
presence
chlormethiazole
(a
CYP2E1-inhibitor;
CMZ)
and/or
EX-527
sirtuin-1
[SIRT1]
inhibitor).
The
culture
medium
was
analyzed
for
protein
abundance.
Cells
mRNA
expression,
SIRT1
abundance,
neutral
lipid
accumulation.
In
parallel,
forkhead
box
O1
[FOXO1],
β-catenin,
peroxisome
proliferator-activated
receptor-α
[PPARα],
lipin-1α
abundance
pharmacological
inhibitors
respective
target
proteins.CYP2E1-dependent
inhibited
amount
detected,
concomitant
with
increased
secretion,
accumulation,
effects
abolished
CMZ.
Analysis
pathways
associated
oxidation
revealed
FOXO1
nuclear
localization
decreased
PPARα,
levels
CYP2E1-expressing
ethanol.
Pharmacological
inhibition
mimicked
ethanol,
while
abrogated
effect
on
accumulation
cells.
failed
alter
accumulation.CYP2E1-dependent
inhibits
SIRT1-FOXO1
signaling,
leads
These
data
suggest
that
released
from
steatotic
could
play
role
promoting
tumor
cell
expansion
setting
represents
potential
therapeutic
intervention.
International Journal of Molecular Sciences,
Год журнала:
2022,
Номер
23(24), С. 15860 - 15860
Опубликована: Дек. 13, 2022
Overnutrition
and
its
sequelae
have
become
a
global
concern
due
to
the
increasing
incidence
of
obesity
insulin
resistance.
A
ketogenic
diet
(KD)
is
widely
used
as
dietary
treatment
for
metabolic
disorders.
Sirtuin1
(SIRT1),
sensor
which
regulates
fat
homeostasis,
modulated
by
interventions.
However,
influence
nutritional
ketosis
on
SIRT1
still
debated.
We
examined
effect
KD
adipose
tissue,
liver,
serum
levels
in
mice.
Adult
C57BL/6J
male
mice
were
randomly
assigned
two
isocaloric
groups
fed
with
either
high-fat
or
normal
chow
(NC)
4
weeks.
Serum
SIRT1,
beta-hydroxybutyrate
(βHB),
glucose,
triglyceride
levels,
well
expression
visceral
(VAT),
subcutaneous
(SAT),
brown
(BAT)
tissues,
measured.
KD-fed
showed
an
increase
βHB
parallel
(r
=
0.732,
p
0.0156),
increased
protein
SAT
VAT.
remained
unchanged
BAT
developed
steatosis.
Normal
glycemia
triglycerides
observed.
Under
KD,
white
phenotypes
show
higher
suggesting
that
one
molecular
mechanisms
underlying
KD's
potential
benefits
health
involves
synergistic
interaction
SIRT1.
Journal of Biomedicine and Biochemistry,
Год журнала:
2023,
Номер
unknown
Опубликована: Июнь 1, 2023
Background
Leukemia
is
a
type
of
cancer
that
affects
the
blood
and
bone
marrow.
This
paper
highlights
role
nicotinamide
adenine
din-
ucleotide
(NAD)
consuming
enzymes
such
as
CD38,
PARP1,
SIRT1
in
patients
with
acute
lymphocytic
leukemia,
myeloid
suffering
from
chronic
leukemia.Materials
methods
Based
on
recent
data.
40
leukemia
(ALL),
(AML),
30
(CML),
healthy
persons
served
controls.
The
enzyme-linked
immunosorbent
assay
(ELISA)
sandwich
technique
was
used
to
detect
serum
levels
SIRT1.Results
In
patient,
groups
compared
control
group,
CD38
con-
centrations
were
discovered
be
considerably
higher
(p
<
0.05),
especially
CML
also
Comparing
patient
it
amounts
PARP1
greater
When
groups'
concentrations
greater,
AML
group
0.05).Conclusion
results
obtained
show
there
reliable
correla-
tion
between
NAD-dependent
are
considered
predictive
indicators
pathological
condition
can
future
treatments.
JHEP Reports,
Год журнала:
2023,
Номер
6(1), С. 100918 - 100918
Опубликована: Сен. 30, 2023
Current
therapies
for
the
treatment
of
alcohol-related
liver
disease
(ALD)
have
proven
largely
ineffective.
Patients
relapse
and
progresses
even
after
transplantation.
Altered
epigenetic
mechanisms
are
characteristic
alcohol
metabolism
given
excessive
acetate
NAD
depletion
play
an
important
role
in
injury.
In
this
regard,
novel
therapeutic
approaches
based
on
modulators
increasingly
proposed.
MicroRNAs,
acting
at
post-transcriptional
level,
appear
to
be
promising
new
targets
ALD.
