Abstract: Objective To study the phosphorylation activity of mitochondrial signal transducer and activator of transcription 3
(STAT3) in the myocardium of rats with selenium deficiency and its association with myocardial injury. Methods Thirty-six
rats were randomized into normal control group (n=18) and selenium deficiency model group (n=18) for feeding with normal
and low-selenium chow, respectively, for 20, 30 and 40 weeks. The cardiac function of the rats was evaluated by carotid artery
intubation, and the damage of cardiac mitochondria was observed under electron microscopy. The cardiac mitochondria were
extracted for assessing succinate dehydrogenase and cytochrome C oxidase activities, and the protein expressions of
phosphorylated and total STAT3 were detected. Results Compared with the corresponding control groups, the rats in the
model group showed significantly decreased cardiac function with obvious structural and functional damage of the cardiac
mitochondria (P<0.05), which aggravated as the low-selenium feeding time extended (P<0.05). The rats in the model group also
showed significantly decreased mitochondrial STAT3 activity (p-STAT3/STAT3) in the myocardium as the low-selenium
feeding time prolonged (P<0.05). Pearson linear correlation analysis showed that the activity of cardiac mitochondrial STAT3
had positive correlations with the left ventricular systolic pressure, maximal increased rate of the left ventricular pressure, and
the activities of succinate dehydrogenase and cytochrome C oxidase (P<0.01). Conclusion Selenium deficiency down-regulates
the activity of mitochondrial STAT3 in rat heart to contribute to cardiac mitochondrial injury and the progression of heart
failure.