Journal of Clinical Medicine,
Год журнала:
2022,
Номер
11(3), С. 572 - 572
Опубликована: Янв. 24, 2022
The
most
challenging
aspect
of
Post-Acute
Sequelae
SARS-CoV-2
Infection
(PASC)
or
Long
COVID
remains
for
the
discordance
between
viral
damage
from
acute
infection
in
recent
past
and
susceptibility
without
clear
evidence
post
infectious
inflammation
autoimmune
reactions.
In
this
communication
we
propose
that
disarray
pericytes
plays
a
central
role
emerge
COVID.
We
assume
are
agents
with
"Triple-A"
qualities,
i.e.,
analyze-adapt
advance,
necessary
sustainability
host
homeostasis.
Based
on
view,
further
suggest
may
provide
model
system
to
integrate
theory
complex
adaptive
systems
explore
new
class
maladies
those
currently
not
well
defined
no
remedies.
Journal of Medical Virology,
Год журнала:
2024,
Номер
96(5)
Опубликована: Май 1, 2024
Nanomedicine
for
treating
post-viral
infectious
disease
syndrome
is
at
an
emerging
stage.
Despite
promising
results
from
preclinical
studies
on
conventional
antioxidants,
their
clinical
translation
as
a
therapy
post-COVID
conditions
remains
challenging.
The
limitations
are
due
to
low
bioavailability,
instability,
limited
transport
the
target
tissues,
and
short
half-life,
requiring
frequent
high
doses.
Activating
immune
system
during
coronavirus
(SARS-CoV-2)
infection
can
lead
increased
production
of
reactive
oxygen
species
(ROS),
depleted
antioxidant
reserve,
finally,
oxidative
stress
neuroinflammation.
To
tackle
this
problem,
we
developed
nanotherapy
based
lipid
(vesicular
cubosomal
types)
nanoparticles
(LNPs)
co-encapsulating
ginkgolide
B
quercetin.
antioxidant-loaded
nanocarriers
were
prepared
by
self-assembly
method
via
hydration
lyophilized
mixed
thin
film.
We
evaluated
LNPs
in
new
vitro
model
studying
neuronal
dysfunction
caused
infection.
examined
key
downstream
signaling
pathways
that
triggered
response
potassium
persulfate
(KPS)
causing
stress-mediated
neurotoxicity.
Treatment
neuronally-derived
cells
(SH-SY5Y)
with
KPS
(50
mM)
30
min
markedly
mitochondrial
while
depleting
levels
both
glutathione
peroxidase
(GSH-Px)
tyrosine
hydroxylase
(TH).
This
led
sequential
activation
apoptotic
necrotic
cell
death
processes,
which
corroborates
crucial
implication
two
proteins
(GSH-Px
TH)
long-COVID
syndrome.
Nanomedicine-mediated
treatment
B-loaded
cubosomes
vesicular
showed
minimal
cytotoxicity
completely
attenuated
KPS-induced
process,
decreasing
apoptosis
32.6%
19.0%
(MO-GB),
12.8%
(MO-GB-Quer),
14.8%
(DMPC-PEG-GB),
23.6%
(DMPC-PEG-GB-Quer)
free
radical
scavenging
replenished
GSH-Px
levels.
These
findings
indicated
GB-LNPs-based
nanomedicines
may
protect
against
regulating
intracellular
redox
homeostasis.
Frontiers in Neurology,
Год журнала:
2023,
Номер
14
Опубликована: Июнь 30, 2023
Severe
acute
respiratory
syndrome
coronavirus
2
(SARS
CoV-2)
causes
disease
2019
(COVID-19),
which
became
a
pandemic
in
late
and
early
2020.
Apart
from
many
other
symptoms
of
this
infection,
such
as
loss
smell
taste,
rashes,
body
aches,
fatigue,
psychological
cardiac
symptoms,
it
also
vasodilation
response
to
inflammation
via
nitric
oxide
release.
SARS
CoV-2
affects
microcirculation,
resulting
the
swelling
damage
endothelial
cells,
micro
thrombosis,
constriction
capillaries,
pericytes
that
are
vital
for
integrity
angiogenesis,
healing
process.
Cytokine
storming
has
been
associated
with
COVID-19
illness.
Capillary
congestion
may
cause
limited
diffusion
exchange
oxygen
lungs
hence
hypoxemia
tissue
hypoxia
occur.
This
perspective
study
will
explore
involvement
capillary
by
their
interference
blood
oxygenation
well
brain
function
persistent
severity
COVID-19.
The
overall
effects
due
COVID-19,
microvascular
damage,
organs
discussed
perspective.
Once
initiated,
vicious
cycle
hypoxia,
function,
turn
damage.
Low
levels
high
cytokines
lead
after-effects
be
form
mood
changes,
anxiety,
depression,
others
need
investigated.
Frontiers in Neurology,
Год журнала:
2024,
Номер
15
Опубликована: Май 30, 2024
Severe
acute
respiratory
syndrome
corona
virus
2
(SARS
CoV-2)
is
the
cause
of
Corona
disease
2019
(COVID-19),
which
turned
into
a
pandemic
in
late
and
early
2020.
SARS
CoV-2
causes
endothelial
cell
destruction
swelling,
microthrombosis,
constriction
capillaries,
malfunction
pericytes,
all
are
detrimental
to
capillary
integrity,
angiogenesis,
healing
processes.
Cytokine
storming
has
been
connected
COVID-19
disease.
Hypoxemia
tissue
hypoxia
may
arise
from
impaired
oxygen
diffusion
exchange
lungs
due
damage
congestion.
This
personal
view
will
look
at
how
inflammation
affect
blood
oxygenation,
cognitive
function,
duration
intensity
The
general
effects
microvascular
injury,
hypoxia,
caused
by
key
organs
also
covered
this
point
view.
Once
initiated,
vicious
cycle
leads
diminished
exacerbates
damage,
increased
hypoxia.
Brain
result
low
levels
high
cytokines
brain
tissue.
In
paper
we
give
summary
direction
with
focus
on
role
neuropeptide
Substance
P.
On
basis
this,
discuss
selected
approaches
question:
“How
P
involved
etiology
results
our
research
could
improve
prevention
or
therapy
corona?
Thereby
pointing
out
post-corona
providing
novel
concepts
for
prevention.
Journal of Clinical Medicine,
Год журнала:
2022,
Номер
11(3), С. 572 - 572
Опубликована: Янв. 24, 2022
The
most
challenging
aspect
of
Post-Acute
Sequelae
SARS-CoV-2
Infection
(PASC)
or
Long
COVID
remains
for
the
discordance
between
viral
damage
from
acute
infection
in
recent
past
and
susceptibility
without
clear
evidence
post
infectious
inflammation
autoimmune
reactions.
In
this
communication
we
propose
that
disarray
pericytes
plays
a
central
role
emerge
COVID.
We
assume
are
agents
with
"Triple-A"
qualities,
i.e.,
analyze-adapt
advance,
necessary
sustainability
host
homeostasis.
Based
on
view,
further
suggest
may
provide
model
system
to
integrate
theory
complex
adaptive
systems
explore
new
class
maladies
those
currently
not
well
defined
no
remedies.