Effects of miR‐190a‐3p on Sevoflurane‐induced postoperative cognitive dysfunction (POCD)

Abstract Postoperative cognitive dysfunction (POCD) is regularly observed in patients postsurgery due to the usage of anesthetics, including Sevoflurane. Research has confirmed the participation of oxidative stress (OS) and inflammation in the pathogenesis of POCD. Recently, the potential therapeutic function of miR‐190a‐3p against cognitive dysfunction has been reported. However, its role and mechanism in POCD are unclear. Our study will focus on the protective property and mechanism of miR‐190a‐3p on POCD to seek potential biomarkers and treatment targets for POCD. The animal model of POCD was constructed by the injection of Sevoflurane, followed by the administration of mimic negative control and miR‐190a‐3p. MiR‐190a‐3p was found to be downregulated in POCD rats. Declined time to explore the platform, swimming distance, and times that rats crossed the platform were observed in POCD rats, accompanied by increased secretion of proinflammatory cytokines, elevated malondialdehyde levels, repressed superoxide dismutase activity, and decreased levels of reduced glutathione, all of which were dramatically reversed by miR‐190a‐3p. Furthermore, the downregulation of nuclear factor erythroid 2‐related factor 2 (Nrf2) and activation of toll‐like receptor 4/nuclear factor‐κB signaling were observed in POCD rats, which were greatly rescued by miR‐190a‐3p. Lastly, the Nrf2 luciferase activity and Nrf2 levels in HT22 cells were extremely improved by miR‐190a‐3p. Collectively, miR‐190a‐3p alleviated Sevoflurane‐induced POCD in rats by repressing OS and inflammation.