Overexpression of long noncoding RNA Malat1 ameliorates traumatic brain injury induced brain edema by inhibiting AQP4 and the NF-κB/IL-6 pathway.

Brain edema is a major traumatic brain injury (TBI)-related neurological complication. In the initiation stage of TBI, brain edema is characterized by astrocyte swelling (cytotoxic edema). We studied the impact of a long noncoding RNA, Malat1, on the TBI-induced astrocyte swelling and brain edema. Our results showed that Malat1 was downregulated in both the TBI rat model and the astrocyte fluid percussion injury (FPI) model, which concurred with brain edema and astrocyte swelling. Overexpression of Malat1 significantly inhibited rat brain edema, meanwhile reducing interleukin-6 (IL-6), nuclear factor-κB (NF-κB), and aquaporin 4 (AQP4) expression after TBI. In addition, overexpression of Malat1 ameliorated FPI-induced astrocyte swelling and reduced IL-6 release. Quantitative real-time polymerase chain reaction and Western blot analysis also corroborated the inhibitory effects of Malat1 on NF-κB and AQP4 expression after FPI. Our results highlighted the protective effects of Malat1 on the TBI-induced brain edema, which were mediated through regulating IL-6, NF-κB, and AQP4 expression. Our study could provide a novel approach for TBI treatment.

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