Inhibition of miR‐378a‐3p Protects Anesthesia‐Induced Hippocampal Neurodegeneration

Ketamine is widely used in pediatric anesthesia, but it may induce cortical neuronal damage, leading to apoptosis, neurofibrillary degeneration, and even cell death. miRNAs can regulate the neurotoxicity induced by ketamine in hippocampal neurons. This article explores the role of miR-378a-3p in ketamine-induced impairments, providing a reference for preventing hippocampal neurodegenerative lesions induced by anesthesia. The expression of miR-378a-3p and AdipoR1 was detected in hippocampal tissues and HT22 cells. To confirm the targeting interaction between miR-378a-3p and AdipoR1, dual-luciferase reporter assays were performed. Cellular viability and apoptosis were also assessed. Ketamine upregulates the expression of miR-378a-3p and downregulates the expression of AdipoR1 in hippocampal tissues and cells, impairing cognitive function in rats. Following ketamine induction, the levels of TNF-α, IL-1β, IL-6, caspase-3, ROS, and MDA are increased, while the level of SOD is decreased in rat hippocampal tissues and cells. Knocking down miR-378a-3p inhibits oxidative stress injury and the release of inflammatory factors by upregulating the expression of AdipoR1. These findings indicate that inhibition of miR-378a-3p protects hippocampal neurons from ketamine-induced damage by upregulating AdipoR1.This suggests that inhibiting miR-378a-3p protects hippocampal neuronal cells from Ketamine-induced damage by upregulating AdipoR1. The study indicates that miR-378a-3p/AdipoR1 axis is a crucial pathway regulating ketamine-induced cognitive impairments and hippocampal neurodegenerative lesions.