Role and Mechanism of miR‐101b‐3p via Targeting <i>TXNIP</i> in Sevoflurane‐Induced Cognitive Impairment in Mice

Sevoflurane may trigger neuroinflammation, thereby leading to cognitive dysfunction. This study aimed to investigate the mechanism of microRNA-101b-3p (miR-101b-3p) in sevoflurane-induced hippocampal neurodegeneration. In this study, 48 male C57BL/6 mice were procured to establish an animal model of cognitive dysfunction. The expression of miR-101b-3p and thioredoxin-interacting protein (TXNIP) was quantified using real-time quantitative polymerase chain reaction (RT-qPCR), and their targeting relationship was validated through a dual-luciferase reporter assay. The Morris water maze test was employed to assess the cognitive ability of mice. The concentrations of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in hippocampal tissues were measured via enzyme-linked immunosorbent assay (ELISA). A detection kit was utilized to evaluate the activity of superoxide dismutase (SOD), malondialdehyde (MDA) content, and reactive oxygen species (ROS) levels. Bcl-2-associated X protein (Bax) and B-cell lymphoma 2 (Bcl-2) proteins were determined by Western blotting. Sevoflurane treatment not only reduced the expression of miR-101b-3p but also concurrently increased the expression of TXNIP. Overexpression of miR-101b-3p was capable of suppressing TXNIP expression and alleviating sevoflurane-induced cognitive dysfunction, inflammatory response, and oxidative stress. Conversely, overexpression of TXNIP reversed these protective effects. Moreover, sevoflurane exposure may induce apoptosis, as indicated by elevated Bax and reduced Bcl-2 expression. However, overexpression of miR-101b-3p inhibited apoptosis, and this effect was counteracted by TXNIP supplementation. Overexpression of miR-101b-3p suppressed the expression of TXNIP, thereby attenuating the inflammatory response and oxidative stress and mitigating sevoflurane-induced cognitive dysfunction.