International immunopharmacology · 2025
A novel postoperative delayed neurocognitive recovery model established based on preoperative rapid eye movement sleep deprivation in adult mice.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Liu Kaixi, Hong Jingshu, Li Yitong, Wang Qian, Dong Rui, Liu Taotao, Guo Xiangyang, Chen Lei, Li Zhengqian
Аннотация
BACKGROUNDS: Postoperative delayed neurocognitive recovery (dNCR) usually occurs in older patients, however, the extremely high cost of older animals has hindered postoperative dNCR research to some extent. Preoperative sleep disturbance increases the risk of postoperative dNCR in patients. Therefore, this study aimed to construct a dNCR model in adult mice based on preoperative sleep disturbance.
METHODS: A modified multiple platform method was used to induce rapid eye movement sleep deprivation (REM-SD), and the surgical model was established by laparotomy in 3-month-old C57BL/6 J mice. The Morris water maze and fear conditioning test were used to assess the cognitive function of mice. Immunofluorescence was used to detect microglia and astrocyte activation, and quantitative real-time PCR was used to measure the mRNA levels of inflammatory cytokines.
RESULTS: Neither laparotomy nor 12 h of REM-SD caused cognitive impairment in mice, but the combination of the two methods induced hippocampus-dependent cognitive dysfunction. Furthermore, hippocampal microglia of mice with 12 h of preoperative REM-SD were polarized to the M1-type, accompanied by increased interleukin-6 and decreased interleukin-10 at the mRNA level.
CONCLUSIONS: We successfully established an adult mouse model of postoperative dNCR based on preoperative REM-SD, which provides an alternative model to explore the pathogenesis and therapeutic measures of dNCR.
METHODS: A modified multiple platform method was used to induce rapid eye movement sleep deprivation (REM-SD), and the surgical model was established by laparotomy in 3-month-old C57BL/6 J mice. The Morris water maze and fear conditioning test were used to assess the cognitive function of mice. Immunofluorescence was used to detect microglia and astrocyte activation, and quantitative real-time PCR was used to measure the mRNA levels of inflammatory cytokines.
RESULTS: Neither laparotomy nor 12 h of REM-SD caused cognitive impairment in mice, but the combination of the two methods induced hippocampus-dependent cognitive dysfunction. Furthermore, hippocampal microglia of mice with 12 h of preoperative REM-SD were polarized to the M1-type, accompanied by increased interleukin-6 and decreased interleukin-10 at the mRNA level.
CONCLUSIONS: We successfully established an adult mouse model of postoperative dNCR based on preoperative REM-SD, which provides an alternative model to explore the pathogenesis and therapeutic measures of dNCR.