Purpose: Research has shown that exposure to anesthesia might increase the risks of
cognitive impairments and learning difficulties. MiR-125b-5p contributed to anesthesia-induced
hippocampal apoptosis. However, the role of miR-125b-5p in sevoflurane-induced cognitive impairments
Methods: Firstly, sevoflurane was used to establish a rat model and cognitive impairment was detected
by the Morris water maze (MWM) test. The hippocampus was observed by HE staining.
The lentivirus-miR-125b-5p antagomiR was transfected into rats to decrease miR-125b-5p. The
interaction between miR-125b-5p and LIM domain kinase 1 (LIMK1) was confirmed by the luciferase
reporter assay. The mRNA and expression levels of related genes and mRNA were examined
by the Quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) and western
Results: Sevoflurane induced the cognitive dysfunction presenting with longer latency time and
few platform crossings in rats. Moreover, miR-125b-5p was observed to be up-regulated in both
sevoflurane-anesthesia rats and sevoflurane-treated SH-SY5Y cells. More importantly, a decrease
in miR-125b-5p could prevent sevoflurane-induced hippocampal apoptosis and inflammation in
rats. Moreover, LIMK1 was the target gene of miR-125b-5p. Interestingly, si-LIMK1 could restore
the sevoflurane-induced cell apoptosis in SH-SY5Y cells, which was alleviated by miR-125b-5p
inhibitor. Finally, the miR-125b-5p inhibitor shortened the time to find the platform and increased
the number of platform crossings compared to sevoflurane-anesthesia rats in the Morris water
maze test. At the same time, the expression of LIMK1 was dramatically increased.
Conclusion: Altogether, these findings suggested that miR-125b-5p inhibitor could protect against
the sevoflurane-induced cognitive impairments by targeting LIMK1.