Ecotoxicology and Environmental Safety,
Год журнала:
2024,
Номер
280, С. 116587 - 116587
Опубликована: Июнь 14, 2024
Early
cyanobacterial
blooms
studies
observed
that
exposure
to
blue-green
algae
led
fish
gills
impairment.
The
objective
of
this
work
was
evaluate
the
toxic
mechanisms
exudates
Microcystis
aeruginosa
(MaE)
on
gills.
In
study,
mechanism
MaE
(2×10
Heliyon,
Год журнала:
2024,
Номер
10(7), С. e28917 - e28917
Опубликована: Март 30, 2024
Bisphenol-A
(BPA),
a
pervasive
industrial
chemical
used
in
polymer
synthesis,
is
found
numerous
consumer
products
including
food
packaging,
medical
devices,
and
resins.
Detectable
majority
of
the
global
population,
BPA
exposure
occurs
via
ingestion,
inhalation,
dermal
routes.
Extensive
research
has
demonstrated
adverse
health
effects
BPA,
particularly
its
disruption
immune
endocrine
systems,
along
with
genotoxic
potential.
This
review
focuses
on
complex
relationship
between
NOD-like
receptor
protein
3
(NLRP3)
inflammasome,
multiprotein
central
to
inflammatory
disease
processes.
We
examine
how
induces
oxidative
stress
through
generation
intracellular
free
radicals,
subsequently
activating
NLRP3
signaling.
The
mechanistic
details
this
process
are
explored,
involvement
signaling
cascades
such
as
PI3K/AKT,
JAK/STAT,
AMPK/mTOR,
ERK/MAPK,
which
implicated
inflammasome
activation.
A
key
focus
wide-ranging
organ
toxicities
associated
exposure,
hepatic,
renal,
gastrointestinal,
cardiovascular
dysfunction.
investigate
immunopathogenesis
molecular
pathways
driving
these
injuries,
highlighting
interplay
among
stress,
inflammasome.
Finally,
explores
emerging
concept
targeting
potential
therapeutic
strategy
mitigate
stemming
from
exposure.
work
integrates
current
knowledge,
emphasizes
mechanisms,
promotes
further
into
NLRP3-targeted
interventions.
Investigative Ophthalmology & Visual Science,
Год журнала:
2025,
Номер
66(3), С. 44 - 44
Опубликована: Март 20, 2025
Purpose:
This
study
aims
to
explore
the
therapeutic
efficacy
of
evodiamine
(EVO)
in
treatment
dry
eye
disease
(DED).
Methods:
Mouse
models
DED
was
developed
using
benzalkonium
chloride
drops
and
subcutaneous
atropine
injections.
Corneal
epithelial
defects
were
assessed
by
fluorescein
sodium
staining,
tear
secretion
measured
with
phenol
red
thread
test.
For
vitro
model,
human
corneal
cells
cultured
a
chloride–enriched
medium.
Phenotypic
mechanistic
analyses
conducted
real-time
quantitative
PCR,
Western
blotting,
flow
cytometry,
immunofluorescence
staining.
Results:
The
administration
EVO
significantly
enhanced
mice,
ameliorated
ocular
surface
damage,
decreased
expression
inflammatory
factors,
increased
density
conjunctival
goblet
cells.
Furthermore,
reduced
oxidative
stress
promoting
autophagy.
Mechanistically,
EVO-induced
autophagy
mediated
via
p53/mammalian
target
rapamycin
pathway.
Conclusions:
These
findings
suggest
that
is
potential
agent
for
DED,
its
beneficial
effects
attributed
activation
through