AI Article Synopsis
- The study investigates how blocking IKK, a key player in inflammation, can reduce heart damage after a heart attack using a rat model.
- After occlusion of the left coronary artery, rats treated with the IKK inhibitor IMD-0560 showed improved heart function and less tissue damage compared to control.
- The findings suggest that inhibiting IKK could be an effective therapy to prevent harmful heart remodeling following ischemic events.
Article Abstract
Objective: Amplification of inflammatory response in the non-infarct area plays an important role in the pathogenesis of ventricular remodeling after myocardial ischemia. Activation of nuclear factor-kappa B (NF-kappaB) is involved in this amplification through a positive feedback loop of pro- inflammatory cytokines. We investigated the efficacy of IKK blockade with IMD-0560, a novel inhibitor of IKK, in a rat myocardial ischemia model.
Methods/results: Left coronary artery occlusion (28 days) was carried out in Sprague-Dawley rats. Daily intraperitoneal injections of IMD-0560 (5 mg/kg) were done after the operation. Treatment with IMD-0560 significantly improved cardiac function as indicated by the preservation of fractional shortening and lower serum brain natriuretic peptide level. Histological analysis showed that IMD-0560 treatment suppressed thinning in the infarcted area compared with vehicle-treated hearts. Moreover, in situ zymography showed matrix metalloprotease-9 activity was inhibited in the infarct area.
Conclusion: We revealed that the IKK blockade is potent for the suppression of chronic ventricular remodeling after myocardial ischemia.
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| http://dx.doi.org/10.1517/14728220802551140 | DOI Listing |
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