LncRNA Mir155hg Knockdown Attenuates Inflammation and Cognitive Impairment through regulating the NF-κΒ signaling pathway in a Rat Model of Status Epilepticus

Abstract

Status epilepticus (SE) is a common neurological emergency that may lead to permanent brain damage or death. Microglia-mediated inflammation play a significant role in the pathogenesis of SE. As precursor of miR-155, long non-coding RNA (lncRNA) Mir155hg has been characterized as inflammation-related lncRNA in the nervous system. However, the molecular mechanism of how Mir155hg regulate inflammation in SE is still not elucidated. The current study aims to investigate the potential role of Mir155hg in SE-induced inflammation. In vitro experiments, the N-methyl-D-aspartate (NMDA) was used to induce inflammation in primary microglia. In vivo, the SE rat model was established with lithium chloride-pilocarpine. The results demonstrated that lncRNA Mir155hg was highly expressed in NMDA-treated microglia and the hippocampus of SE rats. Down-regulated Mir155hg suppressed inflammatory cytokines (IL-1β, IL-6 and TNF-α) both in microglia and SE rats. Meanwhile, the study confirmed that Mir155hg knockdown decreased the level of NF-κΒ p-p65 via Socs1 in microglia. Animal data indicated that Mir155hg knockdown terminated epileptiform discharges during SE. Furthermore, the study showed that Mir155hg knockdown repressed microglial proliferation, alleviated hippocampal neuron damage, and improved cognitive impairment induced by SE. Taken together, our findings demonstrate that lncRNA Mir155hg regulates the inflammation through the miR-155/Socs1/NF-κΒ axis in SE rat.