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Background  Duchenne muscular dystrophy (DMD) associated cardiomyopathy is a major cause of morbidity and mortality. In an in vitro DMD cardiomyocyte model, nicorandil reversed stress-induced cell injury through multiple pathways implicated in DMD .  We aimed to test the efficacy of nicorandil on the progression of cardiomyopathy in  mdx  mice following a 10-day treatment protocol.    Methods  A subset of  mdx  mice was subjected to low-dose isoproterenol injections over 5 days to induce a cardiac phenotype and treated with vehicle or nicorandil for 10 days. Baseline and day 10 echocardiograms were obtained to assess cardiac function. At 10 days, cardiac tissue was harvested for further analysis, which included histologic analysis and assessment of oxidative stress. Paired student’s t test was used for in group comparison, and ANOVA was used for multiple group comparisons.    Results  Compared to vehicle treated mice, isoproterenol decreased ejection fraction and fractional shortening on echocardiogram. Nicorandil prevented isoproterenol induced cardiac dysfunction. Isoproterenol increased cardiac fibrosis, which nicorandil prevented. Isoproterenol increased gene expression of NADPH oxidase, which decreased to baseline with nicorandil treatment. Superoxide dismutase 2 protein expression increased in those treated with nicorandil, and xanthine oxidase activity decreased in mice treated with nicorandil during isoproterenol stress compared to all other groups.    Conclusions  In conclusion, nicorandil is cardioprotective in  mdx  mice and warrants continued investigation as a therapy for DMD associated cardiomyopathy.    Supplementary Information  The online version contains supplementary material available at 10.1186/s12872-021-02112-4.

Cardioprotective effect of nicorandil on isoproterenol induced cardiomyopathy in the Mdx mouse model