Abstract
This study aims to explore the mechanism of dexmedetomidine (Dex) in improving postoperative cognitive dysfunction (POCD) and postoperative sleep in aged rats through the PI3K/Akt signaling pathway. Splenectomy was used to establish a POCD model in aged rats. Open field test (OFT) and new object recognition test (NORT) were used to observe the cognitive function of rats The awakening and sleep times of rats were recorded. Hematoxylin-eosin, Nissl, and TUNEL staining were adopted to examine histopathological alterations, neuronal cell damage, and apoptosis, respectively; western blot to detect the activation of the PI3K/Akt signaling pathway and the protein level of apoptosis factors Bcl-2, Bax, and cleaved caspase-3; enzyme-linked immunosorbent assay to quantify the concentrations of inflammatory factors IL-6, IL-1β, and TNF-α. On days 1, 7, and 14 post-splenectomy surgery, aged rats exhibited shortened moving distance in OFT, reduced discrimination rate in NORT, prolonged awakening time, and shortened sleep time, while such effect was reversed by further Dex treatment. In addition, neuronal damage, inflammatory response, and apoptosis occurred in the hippocampal CA1 area in aged rats but can be attenuated by Dex treatment. Dex triggered the activation of the PI3K/Akt signaling pathway in the hippocampus in aged rats after surgery, and inhibition of the PI3K/Akt signaling pathway can result in a partial reversal of the alleviating effects observed with Dex treatment. Dex improves POCD and postoperative sleep in aged rats by activating the PI3K/Akt signaling pathway to reduce inflammatory response and apoptosis in the hippocampal CA1 area.
Published Version
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