MiR-210 inhibits apoptosis of cranial nerves in preeclampsia rats through suppressing the TGF-β signaling pathway

OBJECTIVE To explore the protective effect of micro ribonucleic acid (miR)-210 on cranial nerves in rats with preeclampsia (PE) by regulating the transforming growth factor-β (TGF-β) signaling pathway. MATERIALS AND METHODS A total of 36 pregnant Sprague-Dawley rats were randomly divided into normal group (n=12), model group (n=12), and miR-210 mimics group (n=12). The rats were fed normally in the normal group. In the latter two groups, the PE model was established, followed by injection of normal saline or miR-210 mimics via the caudal vein, respectively. The above intervention lasted until 20 d of gestational age in pregnant rats. Then, the systolic blood pressure of the caudal vein was measured. The relative levels of Caspase3, phosphorylated TGF-β (p-TGF-β), and miR-210 were detected via immunohistochemistry, Western blotting, and quantitative Polymerase Chain Reaction (qPCR). Cell apoptosis was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. RESULTS The systolic blood pressure of the caudal vein significantly increased in the other two groups compared with that in the normal group (p<0.05), while it significantly decreased in the miR-210 mimics group compared with that in the model group (p<0.05). The results of immunohistochemistry showed that the positive expression of Caspase3 significantly rose in the other two groups compared with that in the normal group (p<0.05), while it remarkably declined in miR-210 mimics group compared with that in the model group (p<0.05). The results of Western blotting revealed that the protein expression of p-TGF-β was evidently higher in the other two groups than that in the normal group (p<0.05), while it was evidently lower in the miR-210 mimics group than that in the model group (p<0.05). Moreover, it was found via qPCR that the other two groups had remarkably lower relative expression of miR-210 than normal group (p<0.05), while miR-210 mimics group had remarkably higher relative expression of miR-210 than the model group (p<0.05). According to the results of TUNEL assay, the apoptosis rate markedly increased in the other two groups compared with that in the normal group (p<0.05), while it markedly decreased in the miR-210 mimics group compared with that in the model group (p<0.05). CONCLUSIONS MiR-210 inhibits apoptosis via suppressing the TGF-β signaling pathway, thereby exerting a protective effect on cranial nerves in PE rats.