Inhibition of Rhoa/Rho Kinase by Ibuprofen Exerts Cardioprotective Effect against Ischemic Reperfusion Injury in Rats

Ischemic Reperfusion Injury is the main cause of mortality globally, researchers are concentrating their efforts on heart protection. Ibuprofen inhibits rho-kinase, a downstream effector of a protein implicated in Ischemic Reperfusion Injury. The goal of this study is to deter Ischemic Reperfusion Injuryne whether ibuprofen has a cardioprotective effect in rats. In an experimental animal, Ischemic Reperfusion Injury was produced by undergoing coronary artery ligation operations. The rats were rando Ischemic Reperfusion Injuryzed into six groups: (I) Normal; (II) model; (III) Sham; (IV-VI) ISO þ ibuprofen (30, 60 and 90 mg/kg p.o). At the end of surgery Langendorff, cardiac marker enzymes, electrolytes, anti-oxidants and gene expression of ROCK-1 were investigated. Pre-treatment with ibuprofen (30, 60, 90 mg/kg, p.o.) for 21 days normalise Blood pressure and improved the ECG pattern, left ventricular function by avoiding ROCK-mediated damage, and prevented the rise in CK-MB, LDH, and Troponin-I and electrolyte level by maintaining cellular integrity. Further, ibuprofen downregulate the mRAN expression of ROCK-1 and preserved the cellular architecture of myocardial tissue. Ibuprofen provided cardioprotection in a model of myocardial infarction, by restoring most of the altered physical, physiological, bioche Ischemic Reperfusion Injurycal, haemodyna Ischemic Reperfusion Injuryc parameters, antioxidant status, and histological changes and by inhibiting ROCK-1 mRNA expression.