Zhang Xiaojia, Zhang Binsen, Qin Xiaoyu, Tang Lu, Wang Chunai
The First Clinical Medical College, Gansu University of Chinese Medicine, Lanzhou, Gansu, China.
Anesthesia and Pain Medical Center, Gansu Hospital of Traditional Chinese Medicine, Lanzhou, Gansu, China.
J Cell Mol Med. 2025 Feb;29(4):e70436. doi: 10.1111/jcmm.70436.
Postoperative cognitive dysfunction (POCD) is common in older adult patients and affects their prognosis. Studies suggested that autophagy and oxidative stress are key factors in the pathogenesis of POCD. This study aimed to determine whether electroacupuncture (EA) pre-treatment improves POCD in aged rats and the underlying mechanisms. We established a model of POCD by using propofol anaesthesia and caesarean section in aged mice and assessed whether electroacupuncture at the Baihui and Neiguan points modulates autophagy and oxidative stress involved in the pathological process of POCD. The Morris water maze test assessed postoperative cognitive function. Oxidative stress was assessed using flow cytometry and enzyme-linked immunosorbent assay (ELISA) to determine the levels of superoxide dismutase (SOD), reactive oxygen species (ROS) and malondialdehyde (MDA). Transmission electron microscopy was used to observe the ultrastructure of the hippocampal cord neurons. In addition, protein blotting and quantitative real-time polymerase chain reaction (PCR) assays were performed to assess SIRT1, FOXO1, and autophagy markers at both the protein and mRNA levels. The results showed that anaesthesia/surgery significantly impaired cognitive performance, increased oxidative stress, decreased autophagy in the hippocampus, damaged hippocampal neurones and disrupted the mitochondrial structure in aged rats. EA pre-treatment improved cognitive function, restored neuronal and mitochondrial function, increased Beclin-1 and SIRT1 levels and attenuated oxidative damage and autophagy dysfunction in POCD rats. In conclusion, EA pre-treatment improved POCD in aged rats, and this mechanism may be related to the enhancement of autophagy and the inhibition of oxidative stress through SIRT1/FOXO1 signalling.
术后认知功能障碍(POCD)在老年患者中很常见,并且会影响他们的预后。研究表明,自噬和氧化应激是POCD发病机制中的关键因素。本研究旨在确定电针预处理是否能改善老年大鼠的POCD及其潜在机制。我们通过在老年小鼠中使用丙泊酚麻醉和剖宫产建立了POCD模型,并评估了百会穴和内关穴的电针是否能调节POCD病理过程中涉及的自噬和氧化应激。莫里斯水迷宫试验评估术后认知功能。使用流式细胞术和酶联免疫吸附测定(ELISA)评估氧化应激,以确定超氧化物歧化酶(SOD)、活性氧(ROS)和丙二醛(MDA)的水平。透射电子显微镜用于观察海马神经元的超微结构。此外,进行蛋白质印迹和定量实时聚合酶链反应(PCR)测定,以评估SIRT1、FOXO1和自噬标志物在蛋白质和mRNA水平上的情况。结果表明,麻醉/手术显著损害了老年大鼠的认知能力,增加了氧化应激,降低了海马中的自噬,损伤了海马神经元并破坏了线粒体结构。电针预处理改善了POCD大鼠的认知功能,恢复了神经元和线粒体功能,增加了Beclin-1和SIRT1水平,并减轻了氧化损伤和自噬功能障碍。总之,电针预处理改善了老年大鼠的POCD,其机制可能与通过SIRT1/FOXO1信号增强自噬和抑制氧化应激有关。