Key result
Cilostazol protected myocardial cells in ischemia-reperfusion injury, but this effect was reduced in obese compared to normal-weight rats (PAI-1 3.7 vs 2.4 ng/mL, p=0.029).
Why the study?
The study was conducted to determine the protective effect of cilostazol on the myocardium in obese Wistar rats subjected to induced ischemia-reperfusion injury.
Does cilostazol protect the myocardium from ischemia-reperfusion injury in obese Wistar rats?
Does cilostazol protect the myocardium from ischemia-reperfusion injury in obese Wistar rats?
Cilostazol demonstrates protective effects against myocardial ischemia-reperfusion injury by decreasing inflammation, though this benefit is attenuated in the setting of obesity.
Answers are grounded in this paper and cite their sources.
May support cilostazol in obese IRI models; leaves open human translation.
OBJECTIVES: This study aims to determine the protective effect of cilostazol on myocardium in obese Wistar rats with induced ischemia-reperfusion injury (IRI). METHODS: Four groups with 10 Wistar rats were included: 1] Sham Group: IRI was not established in normal weight-Wistar rats. 2] Control Group: IRI but no cilostazol in normal weight-Wistar rats. 3] Cilostazol in normal weight-Wistar rats: IRI and cilostazol was administered. 4] Cilostazol in obese- Wistar rats: IRI and cilostazol was administered. RESULTS: Tissue adenosine triphosphate (ATP) levels were significantly higher and superoxide dismutase (SOD) levels significantly lower in the control group than in the sham group and normal weight cilostazol group (p=0.024 and p=0.003). Fibrinogen levels were 198 mg/dL in the sham group, 204 mg/dL in the control group, and 187 mg/dL in the normal-weight cilostazol group (p=0.046). Additionally, plasminogen activator inhibitor-1 (PAI-1) levels were significantly higher in the control group (p=0.047). The level of ATP was significantly lower in the normal-weight cilostazol group than in the obese group (104 vs 131.2 nmol/g protein, p=0.043). PAI-1 level was 2.4 ng/mL in the normal weight cilostazol group and 3.7 ng/mL in the obese cilostazol group (p=0.029). Normal-weight Wistar rats with cilostazol had significantly better histologic outcomes than the control group and obese Wistar rats (p=0.001 and p=0.001). CONCLUSION: Cilostazol has a protective effect on myocardial cells in IRI models by decreasing inflammation. The protective role of cilostazol was reduced in obese Wistar rats compared with normal-weight Wistar rats.
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Demir et al. (2023) studied Ischemia-reperfusion injury (n=40). Cilostazol vs. No cilostazol (control) or sham was evaluated on Tissue ATP, SOD, fibrinogen, PAI-1 levels, and histologic outcomes. Cilostazol protected myocardial cells in ischemia-reperfusion injury, but this effect was reduced in obese compared to normal-weight rats (PAI-1 3.7 vs 2.4 ng/mL, p=0.029).
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