The Function of LINC01187 in Anesthetic-Induced Neurological Impairment by Adsorbing hsa-miR-6069 to Promote IGF2BP3 Expression.

The use of anesthetics may cause damage to the human nervous system, leading to cognitive and motor dysfunction in severe cases. The role of lncRNAs in anesthesia-induced nerve injury have been reported, but their specific regulatory mechanism remains to be explored. By analyzing the GSE160299 and GSE235357 datasets, LINC01187 was screened as our target lncRNA. With the aid of bioinformatics methods, hsa-miR-6069 and IGF2BP3 were predicted as possible downstream molecules of LINC01187. Their expressions were detected by RT-qPCR or western blotting. The dual-luciferase reporter assay was used to determine the targeted association among them. The CCK-8, Annexin V/PI staining, and ROS detection kit were used to evaluate the viability, apoptosis, and oxidative damage of cells. The Rota-Rod and Morris water maze tests were used to measure the motor and learning abilities of rats. LINC01187 showed a low expression in propofol (PPF)- or ketamine (KTM)-treated human cortex neuron cells (hCNCs) and in the hippocampal tissues of KTM-treated rats. Overexpression therapy with LINC01187 alleviated the damage caused by KTM to the motor and learning abilities of rats. LINC01187 targeted hsa-miR-6069 and downregulated it. Hsa-miR-6069 inhibited IGF2BP3 expression by binding to its mRNA. The overexpression of LINC01187 rescued the viability decrease, apoptosis increase, and oxidative damage in PPF/KTM-induced hCNCs by inhibiting hsa-miR-6069 to promote IGF2BP3 expression. In conclusion, intrathecal injection therapy of the LINC01187 vector restored the impairment of motor and learning abilities in KTM-treated rats. LINC01187 protected nerve cells and rats from anesthetic-induced impairment by regulating the hsa-miR-6069/IGF2BP3 axis.