Frontiers in Endocrinology,
Год журнала:
2021,
Номер
12
Опубликована: Ноя. 29, 2021
Mesenchymal
stem
cell-derived
exosomes
have
been
under
investigation
as
potential
treatments
for
a
diverse
range
of
diseases,
and
many
animal
clinical
trials
achieved
encouraging
results.
However,
it
is
well
known
that
the
biological
activity
key
to
their
therapeutic
properties;
however,
till
date,
has
not
completely
understood.
Previous
studies
provided
different
explanations
mechanisms
exosomes,
including
anti-inflammatory,
immunomodulatory,
anti-aging
mechanisms.
The
pathological
effects
oxidative
stress
often
include
organ
damage,
inflammation,
disorders
material
energy
metabolism.
evidence
gathered
from
research
involving
models
indicates
antioxidant
properties,
which
can
also
explain
anti-inflammatory
cytoprotective
effects.
In
this
study,
we
summarized
in
vivo
vitro
models,
evaluated
anti-oxidant
by
demonstrating
direct
reduction
excessive
reactive
oxygen
species
(ROS),
promotion
intracellular
defence
anti-oxidative
stress,
immunomodulation
inhibiting
excess
ROS,
alteration
mitochondrial
performance.
Exosomes
exert
properties
regulating
redox
environment
explains
variety
be
preserved
among
species.
As
the
production,
usage,
and
disposal
of
plastics
increase,
microplastics
generated—plastic
particles
smaller
than
5
mm—increases,
exacerbating
environmental
pollution.
In
turn,
various
organisms
become
increasingly
exposed
to
contaminated
environments,
potentially
affecting
humans
through
food
chain.
Crucial
findings
from
in
vivo
experiments
indicate
histopathological
changes
caused
by
impact
morphology
physiological
function
organisms.
This
study
describes
induced
across
circulatory,
nervous,
digestive,
respiratory,
reproductive
systems
explains
associated
functional
alterations.
Except
nervous
system,
main
morphological
involve
degenerative
throughout
body,
such
as
apoptosis,
inflammation,
fibrosis.
Most
were
inflammatory
responses
microplastics,
leading
fibrosis
subsequent
impairments.
Various
studies
confirm
that
stimulate
cells,
increased
reactive
oxygen
species
cell
death.
Consequently,
these
impair
related
systemic
functions.
review
highlights
fundamental
organs
cells
due
discusses
limitations
involving
showing
no
changes.
Frontiers in Pharmacology,
Год журнала:
2022,
Номер
13
Опубликована: Сен. 5, 2022
Inflammation
and
oxidative
stress
lead
to
various
acute
or
chronic
diseases,
including
pneumonia,
liver
kidney
injury,
cardiovascular
cerebrovascular
metabolic
cancer.
Ginseng
is
a
well-known
widely
used
ethnic
medicine
in
Asian
countries,
ginsenoside
Rg3
saponin
isolated
from
Panax
ginseng
C.
A.
Meyer,
notoginseng,
quinquefolius
L.
This
compound
has
wide
range
of
pharmacological
properties,
antioxidant
anti-inflammatory
activities,
which
have
been
evaluated
disease
models
inflammation
stress.
can
attenuate
lung
inflammation,
prevent
function
damage,
mitigate
neuroinflammation,
cerebral
myocardial
ischemia–reperfusion
improve
hypertension
diabetes
symptoms.
The
multitarget,
multipathway
mechanisms
action
gradually
deciphered.
review
summarizes
the
existing
knowledge
on
effects
underlying
molecular
Rg3,
suggesting
that
may
be
promising
candidate
drug
for
treatment
diseases
with
inflammatory
conditions.
International Journal of Molecular Sciences,
Год журнала:
2023,
Номер
24(3), С. 2365 - 2365
Опубликована: Янв. 25, 2023
Osteoarthritis
(OA)
is
a
degenerative
joint
disease
characterized
by
low-grade
inflammation
and
cartilage
degradation.
Dendrobine
(DEN)
reported
to
inhibit
oxidative
stress
in
some
diseases,
but
its
role
chondrocyte
senescence
OA
progress
has
not
yet
been
elucidated.
Our
study
aimed
explore
the
protective
effects
of
DEN
on
both
vitro
vivo.
We
found
that
inhibited
extracellular
matrix
(ECM)
degradation
promoted
ECM
synthesis.
Meanwhile,
senescence-associated
secretory
phenotype
(SASP)
factors
expression
IL-1β-treated
chondrocytes.
Furthermore,
improved
mitochondrial
function
reduced
production
intracellular
reactive
oxygen
species
(ROS).
Also,
suppressed
IL-1β-induced
activation
NF-κB
pathway.
Further,
using
NAC
(ROS
inhibitor),
we
might
cascades
reducing
ROS.
Additionally,
X-ray,
micro-CT,
histological
analyses
vivo
demonstrated
significantly
alleviated
inflammation,
degradation,
subchondral
alterations
progression.
In
conclusion,
inhibits
SASP
chondrocytes
progression
via
ROS/NF-κB
axis,
which
provides
innovative
strategies
for
treatment
OA.
Nature Communications,
Год журнала:
2025,
Номер
16(1)
Опубликована: Янв. 9, 2025
Liver
fibrosis
is
a
critical
liver
disease
that
can
progress
to
more
severe
manifestations,
such
as
cirrhosis,
yet
no
effective
targeted
therapies
are
available.
Here,
we
identify
ATF4,
master
transcription
factor
in
ER
stress
response,
promotes
by
facilitating
response-independent
epigenetic
program
hepatic
stellate
cells
(HSCs).
Unlike
its
canonical
role
regulating
UPR
genes
during
stress,
ATF4
activates
epithelial-mesenchymal
transition
(EMT)
gene
under
fibrogenic
conditions.
HSC-specific
depletion
of
suppresses
vivo.
Mechanistically,
TGFβ
resets
orchestrate
unique
enhancer
for
the
transcriptional
activation
pro-fibrotic
EMT
genes.
Analysis
human
data
confirms
strong
correlation
between
HSC
expression
and
progression.
Importantly,
small
molecule
inhibitor
targeting
translation
effectively
mitigates
fibrosis.
Together,
our
findings
mechanism
promoting
reveal
new
opportunities
treating
this
otherwise
non-targetable
disease.
lacks
treatments.
This
study
reveals
drives
activating
pharmacological
inhibition
reduces
fibrosis,
offering
an
opportunity
therapies.
Liver
fibrosis
is
a
very
complicated
dynamic
process
where
several
immune
cells
are
involved.
Both
innate
and
adaptive
immunity
implicated,
their
interplay
always
present.
Multi-directional
interactions
between
liver
macrophages,
hepatic
stellate
(HSCs),
cells,
cytokines
important
for
the
induction
perpetuation
of
fibrosis.
Detailed
studies
proteomics
transcriptomics
have
produced
new
evidence
role
individual
in
cirrhosis.
Most
these
controlled
by
various
checkpoints
whose
main
function
to
maintain
homeostasis
implicated
cells.
Recent
indicates
that
involved
In
particular,
programmed
cell
death
protein
1
(PD-1),
death-ligand
(PD-L1),
cytotoxic
T
lymphocyte-associated
antigen
4
(CTLA-4)
been
investigated,
particularly
after
availability
checkpoint
inhibitors.
Their
activation
leads
exhaustion
CD4+ve
CD8+ve
promotion
this
review,
current
pathogenesis
immunological
abnormalities
discussed.
The
recent
data
on
involvement
identified
as
possible
targets
future
interventions.