INSULIN-LIKE GROWTH FACTOR-I DECREASES APOPTOTIC CELL DEATH, BUT NOT PROAPOPTOTIC PROTEIN EXPRESSION IN A TRANSIENT FOREBRAIN ISCHEMIA-REPERFUSION MODEL IN THE RAT

Year 2001, Volume: 14 Issue: 3, 147 - 153, 03.12.2016

Nazire Afşar Sevinç Aktan Dilek İnce-günal

Abstract

Objective: Cerebral ischemia results in both
necrotic and apoptotic cell death. It has been
suggested that approaches directed at disrupting
the apoptotic process and expression of
proapoptotic proteins might be beneficial for
preserving functional neuronal tissue after an
ischemic insult. The aim was to evaluate the
presence of apoptotic cell death and the pattern
of expression of proapoptotic protein (bax) in a
transient forebrain cerebral ischemia model and
to observe the potential benefits of a
neurotrophic factor IGF-I on these parameters.
Methods: Female/male Wistar rats weighing
200-240g were subjected to transient forebrain
ischemia by bilateral carotid artery occlusion
combined with systemic hypotension for 10
minutes. Three reperfusion periods were
performed as 1h, 24h and 7 days. The
experiment was then conducted in two arms: in
group I (n=6 for each reperfusion group),
intracisternal injection of vehicle or 10 pg/rat of
IGF-I was performed at all reperfusion periods,
and these rats were evaluated for the presence
of apoptosis and bax protein expression. Group II
(n=4 for each reperfusion group) was evaluated
for protein oxidation at the three reperfusion
periods.
Results: Apoptosis was significantly higher
(p<0.01) in the vehicle group compared to the
sham group, and IGF-I treatment resulted in a
significant decrease of apoptosis compared to
the vehicle treated group at 24 hour reperfusion.
Moreover, a peak in apoptotic cell death at 24
hour reperfusion was observed, however
remaining just short of significance (p = 0.0730).
No difference in bax protein expression and
protein oxidation could be demonstrated
between reperfusion periods and after IGF-I use.
Conclusion: 10pg/rat of IGF-I produces a
significant suppression in apoptotic cell death at
24 hours reperfusion following transient forebrain
ischemia.
Key Words: IGF-I, Apoptosis, Rat, Forebrain
ischemia.

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