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.