{"title":"西洛他唑对肥胖Wistar大鼠缺血再灌注损伤模型心肌的影响。","authors":"Tolga Demir, Mazlum Sahin, Fatma Tugba Ilal Mert, Fatma Sarac","doi":"10.2174/1570161121666230502141044","DOIUrl":null,"url":null,"abstract":"<p><strong>Objectives: </strong>This study aims to determine the protective effect of cilostazol on myocardium in obese Wistar rats with induced ischemia-reperfusion injury (IRI).</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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).</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":11278,"journal":{"name":"Current vascular pharmacology","volume":" ","pages":"268-273"},"PeriodicalIF":2.8000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Effects of Cilostazol on the Myocardium in an Obese Wistar Rat Model of Ischemia-Reperfusion Injury.\",\"authors\":\"Tolga Demir, Mazlum Sahin, Fatma Tugba Ilal Mert, Fatma Sarac\",\"doi\":\"10.2174/1570161121666230502141044\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objectives: </strong>This study aims to determine the protective effect of cilostazol on myocardium in obese Wistar rats with induced ischemia-reperfusion injury (IRI).</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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).</p><p><strong>Conclusion: </strong>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.</p>\",\"PeriodicalId\":11278,\"journal\":{\"name\":\"Current vascular pharmacology\",\"volume\":\" \",\"pages\":\"268-273\"},\"PeriodicalIF\":2.8000,\"publicationDate\":\"2023-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Current vascular pharmacology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.2174/1570161121666230502141044\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"PERIPHERAL VASCULAR DISEASE\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current vascular pharmacology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.2174/1570161121666230502141044","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"PERIPHERAL VASCULAR DISEASE","Score":null,"Total":0}
Effects of Cilostazol on the Myocardium in an Obese Wistar Rat Model of Ischemia-Reperfusion Injury.
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.
期刊介绍：
Current Vascular Pharmacology publishes clinical and research-based reviews/mini-reviews, original research articles, letters, debates, drug clinical trial studies and guest edited issues to update all those concerned with the treatment of vascular disease, bridging the gap between clinical practice and ongoing research.
Vascular disease is the commonest cause of death in Westernized countries and its incidence is on the increase in developing countries. It follows that considerable research is directed at establishing effective treatment for acute vascular events. Long-term treatment has also received considerable attention (e.g. for symptomatic relief). Furthermore, effective prevention, whether primary or secondary, is backed by the findings of several landmark trials. Vascular disease is a complex field with primary care physicians and nurse practitioners as well as several specialties involved. The latter include cardiology, vascular and cardio thoracic surgery, general medicine, radiology, clinical pharmacology and neurology (stroke units).
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