Objectives To study the phosphorylated expression of signal transducer and activator of transcription 3 (STAT3) in cardiac mitochondria in selenium deficiency rats and its significance.
Methods Sprague-Dawley rats were randomised into normal control group (n = 18) and selenium deficiency model group (n = 18). When rats were fed for 20, 30 and 40 weeks respectively, the cardiac function was detected by carotid artery intubation. The damage of cardiac mitochondria was observed under electron microscopy at the corresponding time points. The cardiac mitochondria were extracted from the rats at the corresponding time points for assessing the enzyme activities of succinate dehydrogenase and cytochrome c oxidase, and detecting the protein expression of phosphorylated and total STAT3.
Results (1) Compared with the corresponding control group, the rats in the model group had notable decreased cardiac function, and significant structure and function damage of cardiac mitochondria (P < 0.05). Moreover, the damage significantly aggravated with the time extension of selenium deficiency (P < 0.05). (2) Compared with the corresponding control group, phosphorylated STAT3 and the ratio of phosphorylated to total STAT3 in cardiac mitochondria in the model group were both significantly decreased, and the reductions were greater as the time of selenium deficiency prolonged (P < 0.05). (3) Pearson linear correlation analysis showed that the the ratio of phosphorylated to total STAT3 in cardiac mitochondria had positive correlations with left ventricular systolic pressure, maximal increased rate of the left ventricular pressure, succinate dehydrogenase and cytochrome c oxidase (P < 0.001).
Conclusions Selenium deficiency down-regulates the phosphorylation activity of mitochondrial STAT3 in the rat heart, which is involved in cardiac mitochondrial injury and the progress of heart failure.