Frontiers in Medicine,
Journal Year:
2024,
Volume and Issue:
11
Published: Aug. 29, 2024
Remarkable
progress
has
been
achieved
in
sepsis
treatment
recent
times,
the
mortality
rate
of
experienced
a
gradual
decline
as
result
prompt
administration
antibiotics,
fluid
resuscitation,
and
implementation
various
therapies
aimed
at
supporting
multiple
organ
functions.
However,
there
is
still
significant
room
for
improvement.
The
septic
patients,
22.5%,
unacceptably
high,
accounting
19.7%
all
global
deaths.
Therefore,
it
crucial
to
thoroughly
comprehend
pathogenesis
order
enhance
clinical
diagnosis
methods.
Here,
we
summarized
classic
mechanisms
progression,
activation
signal
pathways,
mitochondrial
quality
control,
imbalance
pro-and
anti-
inflammation
response,
diseminated
intravascular
coagulation
(DIC),
cell
death,
presented
latest
research
findings
each
mechanism
identify
potential
therapeutic
targets
within
mechanism.
Cell Communication and Signaling,
Journal Year:
2025,
Volume and Issue:
23(1)
Published: Feb. 14, 2025
Sepsis
remains
the
leading
cause
of
death
in
intensive
care
units.
Despite
newer
antimicrobial
and
supportive
therapies,
specific
treatments
are
still
lacking.
Neutrophils
pivotal
components
effector
phase
host
immune
defense
against
pathogens
play
a
crucial
role
control
infections
under
normal
circumstances.
In
addition
to
its
anti-infective
effects,
dysregulation
overactivation
neutrophils
may
lead
severe
inflammation
or
tissue
damage
potential
mechanisms
for
poor
prognosis
sepsis.
This
review
focuses
on
recent
advancements
understanding
functional
status
across
various
pathological
stages
sepsis
explore
by
which
participate
progression
provide
insights
treatment
targeting
neutrophils.
Veterinary Medicine and Science,
Journal Year:
2025,
Volume and Issue:
11(2)
Published: March 1, 2025
ABSTRACT
Life‐threatening
sepsis
with
high
mortality
and
morbidity
is
an
important
cause
of
acute
kidney
injury
myocardial
dysfunction.
In
this
study,
we
investigated
the
protective
effect
Micromeria
congesta
(MC)
against
heart
damage
caused
by
lipopolysaccharide
(LPS)
used
as
a
model.
Control,
LPS,
LPS
+
25
mg/kg
MC
50
groups
were
established
from
rats
for
study.
After
experiment,
tissues
obtained
stained
hematoxylin‐eosin
histopathologic
examination.
Immunohistochemical
staining
was
performed
to
determine
inflammation,
apoptosis,
oxidative
stress
DNA
damage.
IL‐2
CASP‐3
HSP‐27
8‐OHdG
immunopathologic
Histopathologic
examination
showed
that
lesions
in
group
decreased
increasing
doses
MC.
expression
IL‐2,
CASP‐3,
severe
group,
but
severity
these
As
result
it
histopathologically
determined
reduced
LPS‐induced
tissue
addition,
found
protect
reducing
tissue.
conclusion,
seen
effective
However,
concluded
could
be
alternative
drug
strategies
developed
treatment
studies
vivo
including
more
analyses.
Journal of Medicinal Chemistry,
Journal Year:
2024,
Volume and Issue:
67(4), P. 3167 - 3189
Published: Feb. 5, 2024
Mitogen-activated
protein
kinase-interacting
kinases
(MNKs)
and
phosphorylate
eukaryotic
initiation
factor
4E
(p-eIF4E)
play
a
critical
role
in
regulating
mRNA
translation
synthesis
associated
with
the
development
of
cancer,
metabolism,
inflammation.
This
study
undertakes
modification
4-(3-(piperidin-4-yl)-1H-pyrazol-5-yl)pyridine
structure,
leading
to
discovery
4-(3-(piperidin-4-yl)-1H-pyrazol-5-yl)-1H-pyrrolo[2,3-b]pyridine
(D25)
as
potent
selective
MNK
inhibitor.
D25
demonstrated
inhibitory
activity,
IC50
values
120.6
nM
for
MNK1
134.7
MNK2,
showing
exceptional
selectivity.
inhibited
expression
pro-inflammation
cytokines
RAW264.7
cells,
such
inducible
NO
synthase,
cyclooxygenase-2,
interleukin-6
(IL-6).
In
lipopolysaccharide-induced
sepsis
mouse
model,
significantly
reduced
p-eIF4E
spleen
tissue
decreased
tumor
necrosis
α,
interleukin-1β,
IL-6,
it
also
production
reactive
oxygen
species,
resulting
improved
organ
injury
caused
by
suggests
that
may
provide
potential
treatment
sepsis-associated
acute
injury.
American Journal of Reproductive Immunology,
Journal Year:
2024,
Volume and Issue:
91(2)
Published: Feb. 1, 2024
Abstract
Problem
Endometritis
is
a
common
disease
that
affects
dairy
cow
reproduction.
Autophagy
plays
vital
role
in
cellular
homeostasis
and
modulates
inflammation
by
regulating
interactions
with
innate
immune
signaling
pathways.
However,
little
known
about
the
regulatory
relationship
between
autophagy
bovine
endometrial
epithelial
cells
(BEECs).
Thus,
we
aimed
to
determine
of
inflammatory
response
BEECs.
Methods
Study
In
present
study,
expression
levels
proinflammatory
cytokines
were
measured
quantitative
real‐time
polymerase
chain
reaction.
Changes
nuclear
factor‐κB
(NF‐κB)
pathway
determined
using
immunoblotting
immunocytochemistry.
The
induction
autophagosome
formation
was
visualized
transmission
electron
microscopy.
Results
Our
results
demonstrated
activation
inhibited
LPS‐treated
BEECs,
while
NF‐κB
mRNA
IL‐6,
IL‐8,
TNF‐α
increased.
Furthermore,
blocking
inhibitor
chloroquine
increased
factor
Conversely,
agonist
rapamycin
downregulated
factors.
Conclusions
These
data
indicated
LPS‐induced
related
inhibition
may
represent
novel
therapeutic
strategy
for
eliminating
Journal of Cellular Physiology,
Journal Year:
2024,
Volume and Issue:
239(11)
Published: June 18, 2024
Sepsis
is
a
systemic
inflammatory
reaction
caused
by
infection,
and
severe
sepsis
can
develop
into
septic
shock,
eventually
leading
to
multiorgan
dysfunction
even
death.
In
recent
years,
studies
have
shown
that
mitochondrial
damage
closely
related
the
occurrence
development
of
sepsis.
Recent
years
seen
surge
in
concern
over
DNA
(mtDNA),
as
anomalies
this
material
lead
cellular
dysfunction,
disruption
aerobic
respiration,
death
cell.
review,
we
discuss
latest
findings
on
mechanisms
molecular
controlling
mtDNA
release.
We
also
explored
connection
between
misplacement
activation.
Additionally,
propose
potential
therapeutic
targets
for
treatment.
Science of Traditional Chinese Medicine,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 8, 2025
Abstract
Background
Acetaminophen
(APAP)-induced
hepatotoxicity
has
attracted
considerable
attention
in
clinical
settings
due
to
the
limited
treatment
options
available.
Liensinine
stands
out
as
a
key
alkaloid
known
for
its
pharmaceutical
activities.
However,
role
of
liensinine
mitigating
APAP-induced
liver
injury
remains
unclear.
Objective
The
aim
study
was
explore
protective
effects
against
injury.
Methods
C57BL/6
male
mice
were
treated
with
dose
200
mg/kg
N-acetylcysteine
or
varying
doses
(10
20
mg/kg)
seven
consecutive
days.
APAP
(400
mg/kg,
i.g
.)
then
administered
induce
damage
12
hours.
Blood
samples
and
hepatic
tissues
collected
further
analysis.
Liver
enzyme
levels
histopathological
analysis
employed
assess
RNA-seq
conducted
evaluate
dynamic
changes
gene
expression.
Biochemical
assays
used
measure
oxidative
stress
inflammation,
while
TUNEL
assay
performed
hepatocyte
apoptosis.
Results
results
demonstrated
that
administration
mitigated
serum
tissue
resulting
from
overdose.
Transcriptome
revealed
significant
coordinated
genes
related
peroxisome
proliferator-activated
receptor
signaling
pathway,
mitogen-activated
protein
kinase
apoptosis
pathway
response
hepatotoxicity.
expression
alterations
within
these
three
pathways,
associated
stress,
cell
apoptosis,
reversed
by
liensinine,
indicating
potential
alleviating
through
multiple
pathways.
This
suggests
diverse
therapeutic
including
inflammation
suppression,
reduction,
inhibition.
Indeed,
pretreatment
effectively
reduced
inflammatory
cytokines,
indicators,
apoptotic
cells
induced
APAP.
Conclusions
mitigates
multifaceted
providing
anti-inflammatory,
antioxidant,
anti-apoptotic
benefits.
