Science and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangdong, Guangzhou, China; Medical College of Acupuncture-Moxibustion and Rehabilitation, Guangzhou University of Chinese Medicine, Guangdong, Guangzhou, China.
The Affiliated TCM Hospital of Guangzhou Medical University, Guangdong, Guangzhou, China.
Brain Res. 2024 Aug 1;1836:148916. doi: 10.1016/j.brainres.2024.148916. Epub 2024 Apr 10.
Depression is defined by a persistent low mood and disruptions in sleep patterns, with the WHO forecasting that major depression will rank as the third most prevalent contributor to the global burden of disease by the year 2030. Sleep deprivation serves as a stressor that triggers inflammation within the central nervous system, a process known as neuroinflammation. This inflammatory response plays a crucial role in the development of depression by upregulating the expression of inflammatory mediators that contribute to symptoms such as anxiety, hopelessness, and loss of pleasure.
In this study, sleep deprivation was utilized as a method to induce anxiety and depressive-like behaviors in mice. The behavioral changes in the mice were then evaluated using the EZM, EPM, TST, FST, and SPT. H&E staining and Nissl staining was used to detect morphological changes in the medial prefrontal cortical (mPFC) regions. Elisa to assess serum CORT levels. Detection of mRNA levels and protein expression of clock genes, high mobility genome box-1 (Hmgb1), silent message regulator 6 (Sirt6), and pro-inflammatory factors by RT-qPCR, Western blotting, and immunofluorescence techniques.
Sleep deprivation resulted in decreased exploration of unfamiliar territory, increased time spent in a state of despair, and lower sucrose water intake in mice. Additionally, sleep deprivation led to increased secretion of serum CORT and upregulation of clock genes, IL6, IL1β, TNFα, Cox-2, iNOS, Sirt6, and Hmgb1. Sleep.
Sleep deprivation induces anxiety-depressive-like behaviors and neuroinflammation in the brain. Transcription of clock genes and activation of the Sirt6/Hmgb1 pathway may contribute to inflammatory responses in the mPFC.
抑郁症的定义是持续的情绪低落和睡眠模式的紊乱，世界卫生组织预测，到 2030 年，重度抑郁症将成为全球疾病负担的第三大主要贡献因素。睡眠剥夺是中枢神经系统炎症的应激源，这种炎症反应通过上调炎症介质的表达在抑郁症的发展中起着关键作用，这些炎症介质导致焦虑、绝望和快感丧失等症状。
在这项研究中，睡眠剥夺被用作诱导小鼠焦虑和抑郁样行为的方法。然后使用 EZM、EPM、TST、FST 和 SPT 评估小鼠的行为变化。使用 H&E 染色和尼氏染色检测内侧前额叶皮质（mPFC）区域的形态变化。使用 Elisa 评估血清 CORT 水平。通过 RT-qPCR、Western blot 和免疫荧光技术检测时钟基因、高迁移率族蛋白 B1（Hmgb1）、沉默信息调节因子 6（Sirt6）和促炎因子的 mRNA 水平和蛋白表达。
睡眠剥夺导致小鼠对陌生环境的探索减少，绝望状态时间增加，糖水摄入量减少。此外，睡眠剥夺导致血清 CORT 分泌增加和时钟基因、IL6、IL1β、TNFα、Cox-2、iNOS、Sirt6 和 Hmgb1 的上调。睡眠。
睡眠剥夺会引起大脑的焦虑-抑郁样行为和神经炎症。时钟基因的转录和 Sirt6/Hmgb1 途径的激活可能导致 mPFC 中的炎症反应。
