ArticleBMC anesthesiology2026
Role and mechanism of LINC00662 via targeting let-7 g-5p in sevoflurane-induced cognitive impairment in rats.
Article in BMC anesthesiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundThis study was conducted to investigate the role and mechanism of LINC00662 in Sev-induced cognitive impairment by targeting let-7 g-5p.
methodsMouse 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.
resultsSevoflurane 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.
conclusionsThe LINC00662/let-7 g-5p/LIMK2 axis mediates Sev-induced neuronal injury and cognitive dysfunction by regulating neuroinflammation, oxidative stress, and apoptosis.
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