Abstract: Objective To investigate the effect of edaravone on oxidative stress and myocardial fibrosis induced by isoproterenol
in rats. Methods Fifty male SD rats were randomly divided into 5 groups, including a control group, a myocardial fibrosis
model (established by injections of isopropyl adrenaline for 10 days) group, and 3 edaravone groups with edaravone treatment
at low, medium, or high doses for 14 days. After the treatments, the rats were examined for the degree of myocardial fibrosis,
left ventricular mass index (LVMI), collagen volume fraction (CVF), and myocardial contents of collagen I (Col I), collage III
(Col III), hydroxyproline (Hyp), superoxide dismutase (SOD), malondialdehyde (MDA), and nitric oxide (NO); The expression
of transforming growth factor-β1 (TGF-β1) in the myocardial tissues was examined by immunofluorescence assay and Western
blotting. Results Compared with the control rats, the rat models of myocardial fibrosis showed significantly increased CVF
and LVMI (P=0.000), which were lowered by edaravone treatments in a dose-dependent manner (P<0.05). The myocardial
contents of Col I, Col III and Hyp also increased in the model group (P=0.000) and were lowered dose-dependently by
edaravone; the contents of MDA was higher (P=0.000) and SOD and NO were lower in the model group (P=0.000), and
edaravone treatments obviously increased SOD and NO contents (P<0.05). The model rats showed significantly increased
myocardial expression of TGF-β1 (P=0.000), which was markedly lowered by edaravone treatments (P=0.000). The myocardial
content of MDA was positively correlated while SOD and NO were negatively with LVMI, CVF, Col I, Col III and Hyp; TGF-β1
was positively correlated with LVMI, CVF, Col I, Col III, Hyp and MDA but negatively with SOD and NO. Conclusion
Edaravone can relieve oxidative stress and inhibit TGF-β1 activation to ameliorate myocardial fibrosis in rats.