Knockdown of lncRNA BDNF-AS alleviates isoflurane-induced neuro-inflammation and cognitive dysfunction through modulating miR-214-3p.

INTRODUCTION: As one of the most commonly used anesthetics, isoflurane has been demonstrated to possess a variety of protective effects. However, its' neurological impaired effect should be considered during clinical application. Roles of lncRNA BDNF-AS (BDNF-AS) and miR-214-3p in isoflurane-injured microglia and rats were investigated in this study, aiming to disclose the mechanism of isoflurane damage and to provide candidate therapeutic targets. MATERIAL AND METHODS: Isoflurane-induced microglia cells and rat models were established with 1.5% isoflurane. Inflammation and oxidative stress of microglia cells were evaluated with a level of pro-inflammation cytokines, malondialdehyde (MDA), superoxide dismutase (SOD), and nitrite. Cognitive and learning function of rats were assessed with Morris water maze task. Expressions of BDNF-AS and miR-214-3p and their function in the isoflurane-induced microglia cells and rats were estimated with PCR and corresponding transfection. RESULTS: Isoflurane induced significant neuro-inflammation and oxidative stress in the microglia cells. The increased BDNF-AS and the decreased miR-214-3p were noted, and BDNF-AS was found to negatively regulate miR-214-3p in the isoflurane-induced microglia cells. Isoflurane caused cognitive dysfunction in rats, and resulted in a significant inflammatory response. The knockdown of BDNF-AS significantly alleviated the neurological impairment induced by isoflurane, which was reversed by silencing miR-214-3p. CONCLUSIONS: In isoflurane-induced neuro-inflammation and cognitive dysfunction, BDNF-AS showed a significant protective effect on the neurological impairment induced by isoflurane through modulating miR-214-3p.