Role and mechanism of LINC00662 via targeting let-7 g-5p in sevoflurane-induced cognitive impairment in rats

This study was conducted to investigate the role and mechanism of LINC00662 in Sev-induced cognitive impairment by targeting let-7 g-5p. Mouse hippocampal HT22 cells were treated with sevoflurane, and cell viability was assessed by CCK-8. RT-qPCR was performed to detect the expression of LINC00662, let-7 g-5p, and LIMK2. Dual-luciferase and RIP assays verified their binding. The SPF male SD rats were grouped; hippocampal injection of si-LINC00662 or let-7 g-5p antagomir was combined with sevoflurane exposure, followed by MWM for cognitive evaluation. Apoptotic, and inflammatory markers were measured by RT-qPCR. The oxidative stress indicators were detected using corresponding kits. Sevoflurane reduced cell viability, upregulated LINC00662 and LIMK2, and downregulated let-7 g-5p in a dose-dependent and time-dependent manner. LINC00662 directly bound to let-7 g-5p, and let-7 g-5p targeted LIMK2. Silencing LINC00662 reversed Sev-induced cell injury and inflammatory/oxidative stress responses, which were abolished by let-7 g-5p inhibition. In rats, silencing LINC00662 improved sevoflurane-induced cognitive deficits, whereas the let-7 g-5p antagomir worsened them. The LINC00662/let-7 g-5p/LIMK2 axis mediates Sev-induced neuronal injury and cognitive dysfunction by regulating neuroinflammation, oxidative stress, and apoptosis.