Abstract
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.
Graphical Abstract
[PMID: 27356115]
[http://dx.doi.org/10.1111/jar.12667] [PMID: 31482623]
[http://dx.doi.org/10.1159/000489241] [PMID: 29694958]
[http://dx.doi.org/10.3390/ijms20205034] [PMID: 31614478]
[http://dx.doi.org/10.1159/000518879] [PMID: 34547747]
[http://dx.doi.org/10.2174/1570161043476375] [PMID: 15320517]
[http://dx.doi.org/10.1016/j.bbadis.2020.165768] [PMID: 32173461]
[http://dx.doi.org/10.1016/j.ebiom.2020.102884] [PMID: 32653860]
[http://dx.doi.org/10.1016/j.ijcard.2016.06.309] [PMID: 27390990]
[http://dx.doi.org/10.1016/j.amjcard.2010.03.032] [PMID: 20643246]
[http://dx.doi.org/10.2174/1389450123666220913121422] [PMID: 36100990]
[http://dx.doi.org/10.1093/cvr/cvz040] [PMID: 30753344]
[http://dx.doi.org/10.3892/ijmm.2015.2366] [PMID: 26459736]
[http://dx.doi.org/10.1155/2019/4090549] [PMID: 32089885]
[http://dx.doi.org/10.1177/1089253211436350] [PMID: 22368166]
[http://dx.doi.org/10.1007/s10557-021-07187-x] [PMID: 33860901]
[http://dx.doi.org/10.1080/14656566.2018.1515199] [PMID: 30212227]
[http://dx.doi.org/10.1002/bab.1754] [PMID: 30994947]
[http://dx.doi.org/10.1590/S0102-86502013000500007] [PMID: 23702938]
[http://dx.doi.org/10.1590/S0102-86502014001700004] [PMID: 25351151]
[http://dx.doi.org/10.1016/j.ejvs.2008.11.028] [PMID: 19112032]
[http://dx.doi.org/10.6061/clinics/2012(02)13] [PMID: 22358243]
[http://dx.doi.org/10.21470/1678-9741-2020-0651] [PMID: 34673517]
[http://dx.doi.org/10.1002/jcph.1988] [PMID: 34671983]
[http://dx.doi.org/10.2174/0929867327666200903114154] [PMID: 32881655]
[http://dx.doi.org/10.1161/STROKEAHA.120.029454] [PMID: 32646330]
[http://dx.doi.org/10.1016/j.ejphar.2021.174095] [PMID: 33862063]
[http://dx.doi.org/10.14814/phy2.12865] [PMID: 27405971]
[http://dx.doi.org/10.1016/j.mvr.2018.06.003] [PMID: 29940198]
[http://dx.doi.org/10.1080/10409238.2020.1828258] [PMID: 33148057]
[http://dx.doi.org/10.1038/sj.bjp.0704774] [PMID: 12110615]
[http://dx.doi.org/10.1152/ajplung.00409.2001] [PMID: 12060579]
[http://dx.doi.org/10.1097/01.CCM.0000269035.30231.76] [PMID: 17522584]
[http://dx.doi.org/10.1161/ATVBAHA.117.309760] [PMID: 29371242]
[http://dx.doi.org/10.1161/STROKEAHA.116.014091] [PMID: 27470988]
[http://dx.doi.org/10.2119/2004-00032.Aneja] [PMID: 15502883]
[http://dx.doi.org/10.1590/s0102-865020170110000008] [PMID: 29236801]