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

•LncRNA ZFAS1 is highly expressed in TBI mice with secondary CE.•LncRNA ZFAS1 knockout reduces NSS, CWC and neuron numbers.•LncRNA ZFAS1 knockout reduces Bax and caspase-3 levels in TBI mice.•LncRNA ZFAS1 knockout reduces pro-inflammatory cytokines in TBI mice.•LncRNA ZFAS1 may be a target in relieving the secondary injuries after TBI. 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. 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. 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. 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.