Effects of fluvastatin on caveolin-1, HPS90, NADPH oksidaz, RHO-kinase and adma levels in myocardial ischaemia-reperfüsion injury

Ischemia-reperfusion (I / R) injury is the basic pathophysiology of myocardial infarction, cerebral ischemia, stroke, hemorrhagic shock, organ transplantation and thrombolytic therapy. Fluvastatin is a HMG-CoA reductase inhibitor. In addition, endothelial dysfunction healing, antioxidant, antithrombotic, antiatherosclerotic and anti-inflammatory effects of fluvastatin are known. Caveolin-1, HSP90, NADPH oxidase, rho kinase and ADMA are effective molecules in I/R injury by oxidative stress and endothelial nitric oxide pathway. The aim of this study is to investigate the effects of fluvastatin on caveolin-1, HSP90, NADPH Oksidaz, rho-kinase and ADMA levels after myocardial ischaemia-reperfüsion injury For this aim, 27 rats were divided into 3 groups (control, I/R, fluvastatin (10 mg/kg) were administered for 15 days before ischaemia). The left coronary artery was ligated under anesthesia. After this, ischaemia was applied for 30 minute, reperfüsion for 120 minute. ADMA and rho-kinase levels were evaluated with ELISA and HSP90, NADPH oksidaz and caveolin-1 levels evaluated with reverse transcriptase polymerase chain reaction (RT-PCR). HSP90, rho-kinase and ADMA levels increased with ischaemia-reperfüsion in heart tissue. HSP90, rho-kinase and ADMA levels were decreased with fluvastatin. No difference was observed between the groups for caveolin-1 levels. NADPH oxidase levels were decreased significantly in the fluvastatin group. The findings of our study are I/R injury play an important role in the level of ADMA and rho-kinase. The protective effects of statins occur with NO bioavailability and oxidative stress. Key Words: Ischemia / reperfusion, fluvastatin, ADMA