miR-21-5p protects hippocampal neurons of epileptic rats via inhibiting STAT3 expression
Xiaolei Zhang, Xianfeng Li, Bin Li, Chengfeng Sun, Peng Zhang
Abstract
BACKGROUND: Epilepsy is a common chronic neurological disorder worldwide. OBJECTIVES: To investigate the effects of miR-21-5p and signal transducer and activator of transcription-3 (STAT3) expressions on the apoptosis of hippocampal neurons in epileptic rats. MATERIAL AND METHODS: We created a rat model of epilepsy and examined the relationship between miR-21-5p and STAT3 using a bioinformatics website and dual the luciferase reporter (DLR) assay. Real-time quantitative polymerase chain reaction (RT-qPCR) and western blot were used to detect the expression levels of miR-21-5p and STAT3 in hippocampal neurons as well as the protein expression levels of cleaved caspase-3, Bax and Bcl-2, which were related to apoptosis of hippocampal neuron. The apoptosis and survival of hippocampal neurons were detected using TUNEL and Nissl staining. Expressions of inflammatory factors interleukin (IL)-6 and tumor necrosis factor α (TNF-α) in serum were examined with enzyme-linked immunosorbent assay (ELISA). RESULTS: miR-21-5p can bind to STAT3. Compared with the miR-21-5p inhibitor negative control (NC) group, the expression levels of caspase-3 and Bax were higher and the expression level of Bcl-2 was lower in the miR-21-5p inhibitor group, whereas the caspase-3 and Bax levels were lower and Bcl-2 level was higher in the si-STAT3 (interfering STAT3 gene expression by transfecting small interfering RNA) group (all p < 0.05). Treatment with miR-21-5p inhibitor can lead to significant loss and apoptosis of hippocampal neurons, while interfering with STAT3 expression can reduce the loss and apoptosis of the neurons (all p < 0.05). Compared with the miR-21-5p inhibitor NC group, the level of IL-6 was lower in the si-STAT3 group and higher in the miR-21-5p inhibitor group (both p < 0.05). CONCLUSIONS: miR-21-5p can inhibit STAT3 expression and reduce apoptosis and loss of hippocampal neurons and IL-6 level, thereby achieving protective effects on hippocampal neurons of epileptic rats.