Keywords
Doxorubicin; Heart failure; Oxidative stress; Apoptosis; Angiogenesis; Fenofibrate; Superoxide dismutase
Fenofibrate, a ligand and activator of peroxisome proliferator-activated receptor-α (PPAR-α), is used clinically for the treatment of dyslipidemia. Treatment with fenofibrate also reduced the extents of myocardial Z-VDVAD-FMK and collagen deposition in rats infused with angiotensin II [12] as well as ameliorated cardiac dysfunction by suppressing inflammatory responses associated with redox-regulated transcription factors in rats with salt-sensitive hypertension [13]. Polyethylene glycol-conjugated superoxide dismutase (PEG–SOD) had succeeded to prolong plasma half-life of SOD [14], and pretreatment with this conjugate was shown to protect against reperfusion-induced arrhythmias as well as myocardial ischemia-reperfusion injury in animal models [15] and [16]. We have now investigated the mechanism of DOX-induced cardiotoxicity as well as whether fenofibrate or PEG–SOD protects against such toxicity in mice.
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