Abstract
Objective To evaluate the effect of exogenous miR-181b on postoperative cognitive dysfunction (POCD) in mice. Methods A total of 108 clean-grade healthy male C57BL/6 mice, weighing 25-30 g, were divided into 4 groups (n=27 each) using a random number table method: control group (group C), POCD group, miR-181b agonist agomir group (group Ag), and agomir negative control group (group AC). POCD was induced by open tibial fracture in 2.1% isoflurane-anesthetized mice.A total volume of miR-181b agomir 4 μl (0.25 nmol/μl) was injected into bilateral hippocampi at 2 days before establishing the model in group Ag.Agomir negative control solution 4 μl was given at 2 days before establishing the model in group AC.Eighteen mice were selected at days 1, 3 and 7 after surgery, and contextual fear conditioning test was performed to assess cognitive function.Nine mice in each group were sacrificed at 6, 12 and 24 h after surgery (3 mice at each time point), and the hippocampus was isolated for determination of miR-181b expression (by quantitative real-time polymerase chain reaction) and interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) contents (by enzyme-linked immunosorbent assay). Results Compared with group C, the percentage of time spent freezing in the contextual fear conditioning test was significantly decreased at 1, 3 and 7 days after surgery, and the expression of miR-181b was down-regulated and the contents of IL-1β and TNF-α were increased at 6, 12 and 24 h after surgery in POCD and AC groups (P<0.05). Compared with POCD and AC groups, the percentage of time spent freezing in the contextual fear conditioning test was significantly increased 1, 3 and 7 days after surgery, and the expression of miR-181b was up-regulated and the contents of IL-1β and TNF-α were decreased at 6, 12 and 24 h after surgery in group Ag (P<0.05). Conclusion Exogenous miR-181b can mitigate POCD, and the mechanism may be related to inhibiting inflammatory responses in the hippocampus of mice. Key words: MicroRNAs; Cognition disorders; Hippocampus; Neuroinflammation
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