Effect of Dexmedetomidine on Apoptosis and Early Cognitive Dysfunction in Rats Following Propofol Anesthesia

• Published in: Alternative therapies in health and medicine Vol. 30; no. 9; p. 350
• Main Authors: Zhu, Jianbin, Wei, Haixiang, Jiang, Minying, Li, Ting, Wu, Ruizhu, Chen, Hualiang
• Format: Journal Article
• Language: English
• Published: United States 01.09.2024
• Subjects: Animals; Apoptosis - drug effects; Cognitive Dysfunction - drug therapy; Dexmedetomidine - pharmacology; Hippocampus - drug effects; Male; Maze Learning - drug effects; Propofol - pharmacology; Rats; Rats, Sprague-Dawley
• ISSN: 1078-6791

To address the intricate interplay between surgical anesthesia, hippocampal apoptosis, and early cognitive dysfunction in rats, this study delves into the impact of dexmedetomidine (DEX). With a focus on understanding the alterations in the PI3K/Akt pathway, our investigation aims to shed light on the comprehensive dynamics of these processes. Sixty healthy Sprague-Dawley rats were randomly divided into three groups: controls (intraperitoneal saline injection), group A (intraperitoneal propofol injection), and group A + DEX (intraperitoneal propofol and DEX injection), with 20 rats in each group. Cognitive function in the three groups was evaluated using [specify the cognitive function tests, e.g., Morris Water Maze]. The assessment was conducted at various postoperative time points. We employed Hematoxylin-eosin (HE) staining, flow cytometry (FC), Western blot (WB), and real-time fluorescence quantitation polymerase chain reaction (RT-qPCR) to examine hippocampal apoptosis and gene expression. Rats in groups A and A + DEX exhibited higher cognitive scores (NSS) and escape latencies at each postoperative time point, along with a lower proportion of swimming distance (SD) in the target quadrant (TQ) compared to controls. Group A + DEX demonstrated lower NSS and escape latency than controls, accompanied by a higher proportion of SD in TQ. Apoptosis rates of hippocampal cells were higher in groups A and A + DEX than in controls, although they were relatively lower in group A + DEX (P < .05). Regarding gene expression, the relative expression (RE) of Bcl-2, PI3K, pAkt, mRNA expression of Bcl-2 and PI3K, and Bax and caspase3 were altered. Group A + DEX showed higher RE of Bcl-2, PI3K, pAkt, mRNA expression of Bcl-2 and PI3K, and lower Bax and caspase3 than group A (P < .05). For a detailed understanding of the magnitude of these changes, specific values or ranges are provided in the subsequent results section. In conclusion, the combined use of surgical anesthesia with DEX demonstrates a modulatory effect on the PI3K/Akt signaling pathway. This intervention proves effective in reducing hippocampal cell apoptosis post-surgery, thereby alleviating neurological impairments and ameliorating early cognitive dysfunction in rats. Our findings underscore the potential therapeutic impact of DEX in enhancing cognitive outcomes following surgical procedures. The observed reduction in hippocampal cell apoptosis and improvement in cognitive function suggest that DEX may hold promise as a neuroprotective agent in the perioperative setting. These outcomes highlight the clinical relevance of considering DEX as an adjunctive therapy to mitigate cognitive dysfunction associated with surgery. Further investigations and clinical trials are warranted to validate and extend these findings, potentially offering a novel avenue for improving patient outcomes and advancing perioperative care strategies.