摘要：Background: Epilepsy is a neurological disorder of the central nervous system. Inflammation can disrupt the blood-brain barrier, which serves to maintain brain homeostasis. Epilepsy typically occurs in the young and elderly. Further research into epilepsy is needed in order to develop and understand the most appropriate diagnosis and clinical treatment of epilepsy, along with the patho-physiology and mechanism of epilepsy. A well-managed program of research into epilepsy will help to develop a more focused understanding of the occurrence ratio and reasons behind the high prevalence of epilepsy throughout the world. In total, around 50 million people in the world suffer from this neurological disease. The fact is that if the disease is diagnosed properly, sufferers can lead a life seizure-free, as it is estimated that 70% of people with epilepsy recover and lead a normal life. The World Health Organization (WHO) estimates that three quarters of the cases occur in low-income countries. People suffering from epilepsy often face discrimination and stigma in their societies. Objective: To explore the functional role of long non-coding RNA (lncRNA) Hox transcript antisense RNA (HOTAIR) in hippocampal HT-22 after lipopolysaccharide (LPS) stimulation. Methods and materials: An in vitro model was constructed using LPS treatment. Inflammatory cell injury was monitored through changes in cell viability, cell apoptosis and levels of inflammatory cytokines. The HOTAIR level after LPS stimulation was evaluated using the qRT-PCR method. Afterwards, HOTAIR expression was inhibited via cell transfection. The impact of HOTAIR depletion on LPS-induced cell inflammatory injury, and key kinases of NF-κB and MEK/ERK pathways, were investigated. Results: The results of the experiment indicated that LPS treatment led to the upregulation of HOTAIR in HT-22 cells, and LPS-induced cell inflammatory injury was reduced by HOTAIR knockdown. Intriguingly, HOTAIR depletion suppressed the phosphorylated levels of crucial kinases of both NF-κB and MEK/ERK pathways. Conclusions: LPS upregulated HOTAIR, and HOTAIR, can modulate the LPS-induced cell inflammatory injury via NF-κB and MEK/ERK pathways. [Ethiop. J. Health Dev. 2020; 34(3): 205-213] Key words: HOTAIR, LPS, inflammatory injury, neuronal cell, epilepsy, lncRNA, HT-22 cells
