Vitamin C suppresses ovarian pathophysiology in experimental polycystic ovarian syndrome
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Date
2019
Authors
Journal Title
Journal ISSN
Volume Title
Publisher
Elsevier - PATHOPHYSIOLOGY
Abstract
Background:
Polycystic
ovary
syndrome
(PCOS),
also
known
as
the
Stein-Leventhal
syndrome
is
one
of
the
most
common
causes
of
anovulation,
infertility
and
hyperandrogenism
in
women,
affecting
between
5–10
%
of
women
of
reproductive
age
(12–35
years)
worldwide.
Despite
substantial
effort
to
define
the
cause
of
PCOS,
its
pathophysiology
remains
poorly
understood.
Consequently,
determining
the
mech
anisms
of
PCOS
and
the
possible
treatment
is
the
major
goal
of
medical
research
in
endocrine
and
reproductive
physiology.
Aim:
To
investigate
the
mechanism
of
ovarian
metabolic
changes
in
dehydroepiandrosterone
(DHEA)
induced
polycystic
ovary
in
Wistar
rats
treated
with
vitamin
C.
Methods:
Twenty-eight
immature
female
Wistar
rats
weighing
(16–21
g)
were
randomly
divided
into
four
groups
(n
=
7/group):
group
I
served
as
control
and
was
given
water,
group
II
were
injected
with
DHEA
(6
mg/100
g
in
0.2
ml
corn
oil
subcutaneously
to
induce
PCOS
condition),
group
III
received
150
mg/kg
BW
of
Vitamin
C
orally,
group
IV
were
co-administered
with
6
mg/kg
BW
DHEA
in
0.2
ml
of
corn
oil
subcutaneously
and
150
mg/kg
BW
of
Vitamin
C
orally.
All
treatments
lasted
for
15
days.
Twenty-four
hours
after
the
last
administration,
the
rats
were
sacrificed
by
cervical
dislocation.
Blood
samples
and
ovaries
were
collected
for
reproductive
hormonal
analysis,
biochemical
and
histopathological
analysis.
The
expressions
of
mRNA
androgen
receptor
gene
in
the
ovary
were
determined
by
real-time
reverse
transcriptase
polymerase
chain
reaction.
All
data
were
analysed
using
one-way
ANOVA.
Results:
There
was
a
significant
decrease
(p
<
0.05)
in
the
antioxidant
and
metabolic
enzyme
activity
in
the
DHEA
treated
group
compared
with
the
control
group.
DHEA
co-administration
with
Vitamin
C
showed
a
significant
decrease
in
Malondialdehyde,
cytokines
and
Estrogen
and
a
significant
increase
(p
<
0.05)
in
antioxidant
and
metabolic
enzymes
compared
with
DHEA
treated
group
only.
The
histopathological
evaluation
demonstrates
a
reduction
in
cystic
and
atretic
ovaries,
increased
expression
of
Bcl2and
E
Cadherin
with
a
reduction
in
Bax
expression
in
the
group
co-administered
with
DHEA
and
Vitamin
C.
The
DHEA
group
showed
overexpression
of
mRNA
Androgen
Receptor
gene
in
the
ovaries
compared
to
the
control
group.
Conclusion:
This
study
shows
that
Vitamin
C
plays
a
protective
role
against
DHEA-Induced
Polycystic
Ovary
in
Wistar
rats
via
its
antioxidant
and
anti-apoptotic
mechanisms.
Description
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Keywords
Citation
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