Abstract
Background: Despite being one of the main concerns in cardiac surgery, the molecular basis and regulatory mechanisms of postoperative cognitive dysfunction (POCD) are still unclear. In this study, we demonstrate the critical role of miR-138-5p in POCD in mice.
 Methods: We first established an animal model for POCD caused by cardiac surgery. We then used quantitative reverse transcription polymerase chain reaction to examine the expression levels of miR-138-5p and its target mRNAs. The protein level of sirtuin 1 (SIRT1) was determined using Western blot assays. To assess the mice’s recognition abilities, we performed the Morris water maze (MWM) test. Enzyme-linked immunosorbent assays were used to evaluate the expression levels of hippocampal inflammatory cytokines. Finally, we used a luciferase assay to confirm that miR-138-5p directly targeted the mRNA of SIRT1.
 Results: MiR-138-5p was upregulated in the hippocampus of mice following cardiac surgery. Inhibiting miR-138-5p reduced the occurrence of POCD and the hippocampus inflammation in the mice. MiR-138-5p targeted the mRNA of SIRT1, thereby suppressing its expression in the hippocampus of mice following cardiac surgery.
 Conclusion: Our findings suggest that miR-138-5p contributes to cardiac surgery-induced POCD by directly targeting and suppressing the expression of SIRT1 in the hippocampus.
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