The effect of microRNA (miRNA)-19a on gastrointestinal motility in rats with functional dyspepsia was investigated. Fifty adult Sprague-Dawley (SD) rats were randomly divided into 5 groups, 10 rats in each group, one group as the normal group, one group as the model group, and the other three groups were divided into negative control group, miRNA-19a mimic group and miRNA-19a inhibitor group. All rats were intraperitoneally injected with miRNA-19a scramble, miRNA-19a mimic and miRNA-19a inhibitor. Except the normal group, the functional dyspepsia model rat was established by proper clipping tail stimulation. The gastric emptying rate, intestinal propulsive ratio, serum motilin and vasoactive intestinal peptide of rats in each group were measured. The level of miRNA-19a expression in each group was detected by reverse transcription-polymerase chain reaction (RT-PCR). The gastric emptying rate, intestinal propulsive ratio and serum motilin in model group were significantly lower than those in normal group, and vasoactive intestinal peptide was higher in model group than that in normal group (P<0.05). The expression of miRNA-19a in model group was significantly higher than that in normal group (P<0.05). After intraperitoneal injection of miRNA-19a mimic, the expression of miRNA-19a was increased; gastric emptying rate, intestinal propulsive ratio and serum motilin were significantly reduced in model group, and vasoactive intestinal peptide was increased (P<0.05). After intraperitoneal injection of miRNA-19a inhibitor, the expression of miRNA-19a was remarkably decreased; gastric emptying rate, intestinal propulsive ratio and serum motilin were further increased in model group, and vasoactive intestinal peptide was decreased (P<0.05). In conclusion, the expression of miRNA-19a in rats with functional dyspepsia is higher than that in normal rats, and the reduced miRNA-19a expression can ameliorate the gastrointestinal motility in rats with functional dyspepsia.
The present study investigated the effects of myocardial mitochondrial signal transduction and activator of transcription 3 (STAT3), succinate dehydrogenase activity and changes of potassium channel expression on cardiomyocyte apoptosis under low selenium conditions. Primary cultured cardiomyocytes from neonatal mice were divided into the non-toxic control group (0.1 µM sodium selenite) and low selenium treatment group (0.05 µM sodium selenite) according to different selenium concentrations. The expression of mitochondrial STAT3, p-STAT3, p-Kv1.2 potassium channel and apoptosis-related proteins, Bax and Bcl-2, were assessed by immunoblotting. Succinate dehydrogenase activity was measured by spectrophotometry. Flow cytometry was used to detect cardiomyocyte apoptosis. Low selenium treatment reduced the expression of p-STAT3, but did not affect the expression of STAT3. In addition, low selenium treatment reduced the activity of mitochondrial STAT3 and succinate dehydrogenase in cardiomyocytes, leading to injury of myocardial mitochondria. Compared with the control group, low selenium conditions reduced the activity of p-Kv1.2 and reduced the normal electrophysiological function of cardiomyocytes. In the low selenium-treated group, the expression of Bax protein increased, whereas the expression of Bcl-2 protein decreased. The apoptotic rate increased. In conclusion, selenium deficiency in cardiomyocytes leads to decreased potassium channel expression and decreased mitochondrial STAT3 activity and mitochondrial function, which in turn promotes the apoptosis of cardiomyocytes.
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