Introduction
To clarify the potential protective role of cilostazol on rat myocardial
cells with ischemia-reperfusion injury (IRI) models.
Methods
The study was conducted with three groups of 10 Wistar rats (control group,
rats without any coronary ischemia; sham group, rats with coronary ischemia
but without cilostazol administration; and cilostazol group, rats with
coronary ischemia and cilostazol administration). The level of myocardial
injuries was measured by analyzing cardiac troponin T and creatine kinase MB
levels in blood samples. In tissue samples, adenosine triphosphate (ATP),
nitric oxide, superoxide dismutase (SOD), and malondialdehyde were used to
determine the amount of tissue damage. Tissues were stained with
hematoxylin-eosin method, and samples were examined under light
microscope.
Results
The mean level of ATP was 104.4 in the cilostazol group and 149.1 in the sham
group (
P
=0.044). SOD level was significantly higher in the
cilostazol group than in the sham group (2075.3
vs
. 1783.7,
P
=0.043). According to histopathological examination,
all samples were classified as G0 in the control group. In the sham group,
one sample was categorized as G1, six samples as G2, and three samples as
G3. In the cilostazol group, nine samples and one sample were categorized as
G1 and G2, respectively (
P
=0.011).
Conclusion
Cilostazol has beneficial effects on Wistar rats’ myocardial cells in regard
to decreasing inflammatory process, necrosis, and fibrosis. Our findings
revealed that the use of cilostazol significantly decreased ATP and
increased SOD levels in Wistar rats’ myocardial cells after IRI.