Over-expression of TREM2 alleviates cognitive impairment after traumatic brain injury in rats
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Objective To explore the effect of triggering receptor expressed on myeloid cells 2 (TREM2) over-expression on dementia model after traumatic brain injury (TBI) in rats and its possible mechanism. Methods Rats were randomly divided into control group and 2, 5, 7, 14 and 28 days after TBI groups (n=8). RT-qPCR and Western blot were used to detect trem2 mRNA and protein levels in brain tissues. The remaining 32 rats were randomly divided into 4 groups (n=8) : control group, TBI group, TBI+Null group and TBI+ TREM2 group. The TBI+Null group was injected with control lentiviral vector, and the TBI+ TREM2 group was injected with the same amount of lentiviral vector encoding TREM2. The memory function of rats in each group was assessed by Morris water maze, and the expression levels of microglia phenotypes (iNOS and Arg-1), neuroinflammatory related factors (IL-1β, IL-6, IL-4 and IL-10) and cognition-related proteins [amyloid β1-42 (Aβ1-42) and tau] in brain tissues of rats in each group were assessed by RT-qPCR and Western blot. Results Compared with the control group, the expressions of TREM2, TREM2mRNA, mean escape latency, iNOS, IL-1β, IL-6, Aβ1-42 and Tau were increased in TBI group, while the expressions of Arg-1, IL-4 and IL-10 were decreased (P<0.05). TBI+ Trem2 group significantly alleviated the mean escape latency, increased expression of iNOS, IL-1β, IL-6, Aβ1-42 and Tau, and decreased expression of Arg-1, IL-4 and IL-10 (P<0.05). Conclusions TREM2 over-expression can regulate the microglial phenotype in brain tissue of TBI rats, reduce the expression of cognition-related proteins (Aβ1-42, tau), and improve the learning and memory function.