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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 25, No 5, September/October 2014
214
AFRICA
2). While hsp 90 levels increased 1.6-fold in the I/R group, they
decreased significantly in the rosuvastatin group and returned
to control values (Fig. 3). There was no significant difference
between groups in terms of caveolin-1 levels (Fig. 4).
NADPH oxidase levels significantly increased with I/R, and
a limited but statistically significant attenuation was observed
in only the rosuvastatin group (Fig. 5). Similarly, rosuvastatin
treatment was able to significantly attenuate the increase in
rhokinase levels (Fig. 6).
Discussion
Results from this study show that 15-day intraperitoneally
injected rosuvastatin was able to decrease the myocardial injury
caused by I/R. Ischaemia–reperfusion itself increased tissue
NFkB, hsp 90, ADMA, and NADPH levels without significantly
changing caveolin-1 levels. According to our results, rosuvastatin
inhibited changes in levels of NFkB, hsp 90, rhokinase, ADMA
and NADPH oxidase but not caveolin-1 levels in rat cardiac
tissue with induced myocardial I/R.
The beneficial effects of statins have been shown in
cardiovascular diseases, including acute coronary syndromes.
8,18,22
It was reported that rosuvastatin may have protective effects
in I/R injury and these effects could have been mediated by
immunomodulatory and anti-inflammatory effects.
7,17,23
Kuhn
et
al
.
24
showed that myocardial function improved with rosuvastatin
administration for seven days prior to cardiopulmonary bypass
surgery. The protective effects of rosuvastatin regarding
antioxidant and anti-inflammatory properties have also been
reported in brain I/R models.
25
12
11
10
9
8
7
6
5
4
3
2
1
0
Control
IR
Rosuvastatin
ADMA (ng/ml)
Fig. 1.
Effect of rosuvastatin on ADMA levels in myocardial I/R.
Vehicle or rosuvastatin (10 mg/kg) were administered
by intraperitoneal injection for 15 days before ischae-
mia (
n
=
7 in each group). *
p
<
0.05 significantly differ-
ent from control group (one-way analysis of variance
followed by a
post hoc
Tukey HSD test).
2.5
2.0
1.5
1.0
0.5
0.0
Control
IR
Rosuvastatin
NFkB mRNA levels (%)
Fig. 2.
Effect of rosuvastatin on NFkB mRNA levels in
myocardial I/R. Vehicle or rosuvastatin (10 mg/kg)
were administered by intraperitoneal injection for 15
days before ischaemia (
n
=
7 in each group). *
p
<
0.05
significantly different from control group and a;
p
<
0.05
significantly different from IR group (one-way analysis
of variance followed by a
post hoc
Tukey HSD test).
2.0
1.5
1.0
0.5
0.0
Control
IR
Rosuvastatin
Hsp 90 mRNA levels (%)
Fig. 3.
Effect of rosuvastatin on hsp 90 mRNA levels in
myocardial I/R. Vehicle or rosuvastatin (10 mg/kg)
were administered by intraperitoneal injection for 15
days before ischaemia (
n
=
7 in each group). *
p
<
0.05
significantly different from control group and a;
p
<
0.05
significantly different from IR group (one-way analysis
of variance followed by a
post hoc
Tukey HSD test).
1.5
1.0
0.5
0.0
Control
IR
Rosuvastatin
Caveolin-1 mRNA levels (%)
Fig. 4.
Effect of rosuvastatin on caveolin-1 mRNA levels in
myocardial I/R. Vehicle or rosuvastatin (10 mg/kg) were
administered by intraperitoneal injection for 15 days
before ischaemia (
n
=
in 7 each group, one-way analy-
sis of variance followed by a
post hoc
Tukey HSD test).