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Background <p>This study was conducted to investigate the role and mechanism of LINC00662 in Sev-induced cognitive impairment by targeting let-7&#xa0;g-5p.</p> Methods <p>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&#xa0;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&#xa0;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.</p> Results <p>Sevoflurane reduced cell viability, upregulated LINC00662 and LIMK2, and downregulated let-7&#xa0;g-5p in a dose-dependent and time-dependent manner. LINC00662 directly bound to let-7&#xa0;g-5p, and let-7&#xa0;g-5p targeted LIMK2. Silencing LINC00662 reversed Sev-induced cell injury and inflammatory/oxidative stress responses, which were abolished by let-7&#xa0;g-5p inhibition. In rats, silencing LINC00662 improved sevoflurane-induced cognitive deficits, whereas the let-7&#xa0;g-5p antagomir worsened them.</p> Conclusions <p>The LINC00662/let-7&#xa0;g-5p/LIMK2 axis mediates Sev-induced neuronal injury and cognitive dysfunction by regulating neuroinflammation, oxidative stress, and apoptosis.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月20日

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  • Shuang Wu,
  • Hao Chen,
  • Jing Qian,
  • Shiping Wang

摘要

Background

This study was conducted to investigate the role and mechanism of LINC00662 in Sev-induced cognitive impairment by targeting let-7 g-5p.

Methods

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.

Results

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.

Conclusions

The LINC00662/let-7 g-5p/LIMK2 axis mediates Sev-induced neuronal injury and cognitive dysfunction by regulating neuroinflammation, oxidative stress, and apoptosis.