Attenuation of propofol-induced hippocampal neuron damage in developing rats by dexmedetomidine

Abstract

This study explored the mechanism of dexmedetomidine attenuating propofol damage to hippocampal neurons in rats. By constructing rat hippocampal neuron model and carrying out targeted intervention; enzyme linked immunosorbent assay (ELISA) detected IL-1β and IL-18 levels; while Nissl staining observed hippocampus Histopathology; flow cytometry quantitatively analyzed the number of hippocampal neuron cells and apoptosis rate. Moreover, levels of PKA, Caspase-1 and NOD-like receptor thermal protein domain associated protein 3(NLRP3) and corresponding proteins were measured. Results showed that, there were more Nissl bodies in cytoplasm of hippocampal neurons in control group, and distribution in the cytoplasm was relatively uniform. Moreover, IL-1β and IL-18 in model group continued to increase; while dexmedetomidine effectively inhibited apoptosis of hippocampal neurons, which may be related to decreased expression of protein kinase A (PKA). After using PKA inhibitors, apoptosis was significantly inhibited, and when the expression of PKA was reduced, Caspase-1 was down-regulated along with reduced NLRP3 level, which improved the injury of hippocampal neurons. Dexmedetomidine can therefore down-regulate the level of Caspase-1 in hippocampal neurons by inhibiting the PKA signaling pathway, improving apoptosis, reducing the genetic and protein expressions of NLRP3, and slowing down the damage of hippocampal neurons.