LncRNA-UCA1 inhibits the astrocyte activation in the temporal lobe epilepsy via regulating JAK/STAT signaling pathway

This article aimed to reveal the mechanism of Urothelial cancer associated 1 (UCA1) regulated astrocyte activation in temporal lobe epilepsy (TLE) rats via JAK/STAT signaling pathway. A model of TLE was established based on rats via kainic acid (KA) injection. All rats were divided into sham group, KA group, normal control (NC) + KA group and UCA1 + KA group. The Morris water maze was used to test the learning and memory ability of rats, and the expression of UCA1 in hippocampus was determined by qRT-PCR. Surviving neurons were counted by Nissl staining, and expression of glial cells glial fibrillary acidic protein, p-JAK1, and p-STAT and glutamate/aspartate transporter (GLAST) was analyzed by immunofluorescence and Western blot. A rat model of TLE was established by intraperitoneal injection of KA. QRT-PCR and fluorescence study showed that UCA1 inhibited astrocyte activation in hippocampus of epileptic rats. Meanwhile, the MWM analysis indicated that UCA1 improved the learning and memory in epilepsy rats. Moreover, the Nissl staining showed that UCA1 might has protective effect on neuronal injury induced by KA injection. Furthermore, the immunofluorescence and Western blot analysis revealed that the overexpression of UCA1 inhibited KA-induced abnormal elevation of GLAST, astrocyte activation of JAK/STAT signaling pathway, as well as hippocampus of epilepsy rats. UCA1 inhibited hippocampal astrocyte activation and GLAST expression in TLE rats via regulating JAK/STAT signaling, and improved the adverse reactions caused by epilepsy.