Objective To explore the effect of triggering receptor expressed on myeloid cells-2 (TREM2) on cognitive dysfunction after traumatic brain injury (TBI) in rats and its possible mechanism.
Methods Twenty-four rats were randomly divided into sham group (sham operation), TBI group and TBI complicated with TREM2 group (TREM2 overexpression), with 8 rats in each group. TBI rat model was constructed by cortical strike in TBI group and TBI complicated with TREM2 group, and the sham group only opened the bone window. TREM2 overexpression model was constructed by intraventricular injection of adenovirus-associated virus (AAVRH. 10) AAVRH. 10 TREM2. The Sham group and the TBI group were injected with the same amount of AAVRH. 10 Null capsid. After 28 days, Morris water maze was used to evaluate the learning and memory function of rats in each group. Western blot was used to evaluate the expression levels of TREM2 and cognition-related proteins, and Western blot as well as immunofluorescence were used to evaluate the expression levels of autophagy proteins.
Results Compared to the sham group, average escape latency of TBI group was prolonged, cognitive impairment related proteinsamyloid beta (1-42) (Aβ1-42), tau expression, TREM2 expression level, autophagy protein LC3-Ⅱexpression and LC3-Ⅱ/LC3-Ⅰ expressionall increased, P62 expression decreased, the differences of the above indicators were statistically significant (P < 0.05). Compared with TBI group, the average escape latency of rats in the TBI complicated with TREM2 group was shortened, cognitive impairment related proteins (Aβ1-42, tau) was reduced, TREM2 expression, LC3-Ⅱ autophagy protein expression and LC3-Ⅱ/LC3-Ⅰexpression all increased, P62 expression decreased, the differences of the above indicators were statistically significant (P < 0.05).
Conclusion TREM2 overexpression can improve cognitive dysfunction in TBI rats, possibly by mechanism of promoting microglial autophagy.
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