全身性炎症对来自非细菌性内毒素动物模型的神经炎症的影响的证据
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Evidence of the impact of systemic inflammation on neuroinflammation from a non-bacterial endotoxin animal model
背景与目的：全身性炎症反应诱导神经炎症和细胞改变如tau蛋白磷酸化来损害包括学习和记忆在内的认知功能。本研究使用单一模型，无菌剖腹术，来阐述这些变化以及它们在中间阶段对抗炎治疗的反应。
1
方法：在两部分实验中，野生型C57BL / 6N小鼠（雄性，3个月大，25±2g）单独进行七氟醚麻醉或进行剖腹手术。在术后第1天，第3天和第14天评估其认知功能表现，全身和神经炎症反应以及tau蛋白磷酸化。然后评估围术期布洛芬干预（60 mg / kg）对这些变化的影响。
结果：剖腹手术组小鼠在剖腹术后长达14天显示记忆障碍，肝脏，额叶皮质（IL-1β，IL-6和TNF-α）和海马（IL-1β和IL-8）的炎症细胞因子水平初始高。在剖腹手术后14天，尽管大多数循环和常驻细胞因子水平恢复正常，但是大量小胶质细胞和星形胶质细胞在海马的额叶皮质和小胶质细胞中仍然可被激活，以及这两个脑区域中的tau蛋白磷酸化异常。围术期布洛芬能改善认知功能障碍，可减轻全身炎症反应和神经胶质细胞活化，并抑制额叶皮质和海马中的异常tau蛋白磷酸化。
结论：我们的研究结果表明：（1）认知功能障碍与不平衡的促炎和抗炎反应，tau蛋白磷酸化异常和神经胶质细胞增生有关; （2）剖腹手术后认知功能障碍，神经胶质增生和τ蛋白病可以持续很久; （3）抗炎药可以迅速起作用，减轻大脑中的炎症反应，并负面调控神经病理变化，改善认知。
Huang L1, Huang K2, Ning H3
Hispidulin prevents sevoflurane— Induced memory dysfunction in aged rats
Biomed Pharmacother. 2018 Jan;97:412-422. doi: 10.1016/j.biopha.2017.10.142.
Background
Systemic inflammation induces neuroinflammation and cellular changes such as tau phosphorylation to impair cognitive function, including learning and memory. This study uses a single model, laparotomy without any pathogen, to characterize these changes and their responses to anti-inflammatory treatment in the intermediate term
METHODS
In a two-part experiment, wild-type C57BL/6N mice (male, 3 month old, 25 ± 2 g) were subjected to sevoflurane anesthesia alone or to a laparotomy. Cognitive performance, systemic and neuroinflammatory responses, and tau phosphorylation were evaluated on postoperative days (POD) 1, 3, and 14. The effect of perioperative ibuprofen intervention (60 mg/kg) on these changes was then assessed
RESULTS
Mice in the laparotomy group displayed memory impairment up to POD 14 with initial high levels of inflammatory cytokines in the liver, frontal cortex (IL-1β, IL-6, and TNF-α), and hippocampus (IL-1β and IL-8). On POD 14, although most circulating and resident cytokine levels returned to normal, a significant number of microglia and astrocytes remained activated in the frontal cortex and microglia in the hippocampus, as well as abnormal tau phosphorylation in these two brain regions. Perioperative ibuprofen improved cognitive performance, attenuated systemic inflammation and glial activation, and suppressed the abnormal tau phosphorylation both in the frontal cortex and hippocampus。
CONCLUSIONS
Our results suggest that (1) cognitive dysfunction is associated with an unbalanced pro-inflammatory and anti-inflammatory response, tauopathy, and gliosis; (2) cognitive dysfunction, gliosis, and tauopathy following laparotomy can persist well beyond the immediate postoperative period; and (3) anti-inflammatory drugs can act rapidly to attenuate inflammatory responses in the brain and negatively modulate neuropathological changes to improve cognition.
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