Silencing long non-coding RNA zinc finger antisense 1 restricts secondary cerebral edema and neuron injuries after traumatic brain injury.

Abstract Objective To investigate the interaction of long non-coding RNA zinc finger antisense 1 (lncRNA ZFAS1) in secondary cerebral edema (CE) and neuron injuries after traumatic brain injury (TBI) in a mouse model. Methods TBI mouse models was established by free-fall strike. Adeno-associated virus-short hairpin-ZFAS1 was administrated into mice via intracerebral injection to downregulate lncRNA ZFAS1. LncRNA ZFAS1 in mouse brain was examined. Neurological severity score (NSS), cerebral water content (CWC) and lesion volume were measured. The number of TUNEL-positive cells in brain tissue was accessed. Bax and cleaved caspase-3 in brain tissues were measured by western blot analysis, and pro-inflammatory factor levels were detected. Results LncRNA ZFAS1 expression was upregulated in mouse brain tissues 3 days after TBI modelling. After the knockdown of lncRNA ZFAS1, NSS, CWC and lesion volume were decreased, apoptotic gene levels were decreased and pro-inflammatory cytokine levels were reduced, suggesting that lncRNA ZFAS1 knockdown could alleviate TBI-induced brain injuries in mice. Conclusion This study demonstrated that silencing lncRNA ZFAS1 inhibited TBI by quenching apoptosis, reducing inflammatory response and improving the recovery of neurological function in TBI mice. LncRNA ZFAS1 might function as a possible curative management in secondary CE and neuron injury in TBI mice.