Sinapic Acid Ameliorates Oxidative Stress, Inflammation, and Apoptosis in Acute Doxorubicin-Induced Cardiotoxicity via the NF-κB-Mediated Pathway

Figure 3

Effect of sinapic acid (SA) pretreatment on the histopathological changes in the cardiac tissue of DOX-treated rats. Photomicrographs of the myocardium tissue in (a) normal rats (group I) exhibiting normal cardio myofibril architecture (red arrow); (b) DOX-treated rats (group II) exhibiting perivascular cuffing (green arrow) of the vasa vasorum with intimal fibrosis, disrupted medial elastic fibers with diffuse interstitial fibrosis, myocytolysis (orange arrow), and myonecrosis (blue arrow); (c) DOX (15 mg/kg)+SA (20 mg/kg)-treated rats (group III) showing decreased degree of myonecrosis (black arrow) and less infiltration of inflammatory cells; and (d) captopril (CAP; 30 mg/kg)+SA (20 mg/kg)-treated rats displaying reversal of myocardial damage based on the reduction in the degree of necrosis and minor infiltration of inflammatory cells. Heart tissues were stained with hematoxylin and eosin and visualized under a light microscope at 100x magnification.

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