Camellia Tea Saponin Ameliorates 5–Fluorouracil-Induced Damage of HaCaT Cells by Regulating Ferroptosis and Inflammation
Nutrients,
Год журнала:
2025,
Номер
17(5), С. 764 - 764
Опубликована: Фев. 21, 2025
Background/Objective:
Ferroptosis
is
an
iron-dependent
form
of
programmed
cell
death
characterized
by
lipid
peroxidation
products
(LPOs).
A
chemotherapeutic
drug,
5–fluorouracil
(5–FU),
can
induce
epithelial
mucositis
and
favor
drug
synergism
with
erastin
in
ferroptosis.
Camellia
tea
saponin
extract
(TS)
known
to
exert
antioxidative
properties.
This
study
aims
delineate
the
protective
role
TS
mitigating
5–FU-induced
ferroptosis
inflammation
human
keratinocytes.
Methods:
HaCaT
cells
were
induced
5–FU
erastin,
treated
different
doses,
their
viability
was
then
determined.
Levels
cellular
reactive
oxygen
species
(ROS),
LPOs,
labile
iron
pool
(LIP),
glutathione
(GSH),
peroxidase
4
(GPX–4)
activity,
as
well
IL–6,
IL–1β,
TNF–α
levels,
wound
healing
properties
assessed.
Results:
per
se
(at
up
25
µg/mL)
not
toxic
but
unable
restore
baseline
levels.
The
compound
significantly
diminished
increases
ROS,
LIP,
while
restoring
GSH
content
GPX–4
activity.
Additionally,
it
suppressed
cytokine
production
a
concentration–dependent
manner.
Moreover,
exerted
wound-healing
effects
against
skin
injuries
damage
dose
dependently.
Conclusions:
insights
this
work
have
identified
biochemical
mechanisms
using
protect
keratinocyte
inflammation.
highlights
promising
adjunctive
potential
mitigation
management
chemotherapy-induced
mucositis.
Язык: Английский
Mechanistic Insights into Maltol-Mediated Reversal of Postmenopausal Osteoporosis via Regulation of CDK14 Ubiquitination in Macrophages
Journal of Agricultural and Food Chemistry,
Год журнала:
2025,
Номер
unknown
Опубликована: Май 2, 2025
Maltol,
primarily
derived
from
Korean
red
ginseng,
exhibits
anti-inflammatory
properties
by
modulating
macrophage
polarization
and
has
potential
therapeutic
effects
on
postmenopausal
osteoporosis,
a
condition
linked
to
inflammation.
This
study
explored
the
molecular
mechanisms
underlying
maltol's
ability
inhibit
M1
regulate
osteoblast
differentiation
via
macrophage-mediated
pathways.
Using
in
vitro
vivo
models,
we
demonstrated
that
maltol
upregulates
RNF213,
which
inhibits
CDK14-Pdgfrβ
signaling
pathway,
suppressing
reducing
NFκB
phosphorylation
pro-inflammatory
cytokine
production.
Additionally,
decreases
TNFSF12
secretion,
mitigating
estrogen
deficiency-induced
apoptosis
promoting
differentiation.
These
findings
highlight
managing
osteoporosis
other
inflammatory
diseases.
Язык: Английский