Inhibition of miR-1187 attenuates isoflurane-induced cognitive dysfunction in mice via targeting Syp.

BACKGROUND: Isoflurane is a common anesthetic agent that can cause learning and memory impairments. This study aims to elucidate the effects of miR-1187 on isoflurane-induced cognitive dysfunction in mice and uncover its underlying molecular mechanisms. METHODS: An isoflurane-induced animal model was established using male C57BL/6 mice. Learning and memory capabilities of mice were assessed through the Morris water maze test. The expression of miR-1187 and Syp was quantified via quantitative real-time polymerase chain reaction (qRT-PCR). Inflammatory factors (interleukin-1β (IL-1β), IL-6, tumor necrosis factor-α (TNF-α)) levels were measured by enzyme-linked immunosorbent assay (ELISA). Cell viability and apoptosis were determined using the Cell Counting Kit-8 (CCK-8) assay and flow cytometry, respectively. Potential target genes of miR-1187 were screened by bioinformatics prediction and further verified using the dual-luciferase reporter assay. RESULTS: Isoflurane treatment upregulated miR-1187 expression in hippocampal tissues and cells and decreased Syp expression. Isoflurane treatment prolonged escape latency to the hidden platform, shortened residence time in the target quadrant, and elevated the inflammatory cytokines levels in mice. Downregulation of miR-1187 protected mice against isoflurane-induced learning and memory impairments and inflammatory responses. Inhibition of miR-1187 effectively alleviated the decline in neuronal cell viability and attenuated apoptosis and inflammatory response induced by isoflurane. Syp was the target gene of miR-1187. Inhibiting Syp partially counteracted the protective effects of miR-1187 downregulation against neuronal injury and inflammatory responses. CONCLUSION: Inhibiting miR-1187, which targets and regulates Syp, can alleviate neuronal damage and inflammatory responses and thereby ameliorate isoflurane-induced cognitive dysfunction.