七氟醚预处理能改善小鼠脂多糖导致的认知功能障碍
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Sevoflurane preconditioning ameliorates lipopolysaccharide-induced cognitive impairment in mice
背景与目的：全身性炎症诱发脑神经细胞炎症，进而引起急性认知功能障碍。此外，神经元炎症是术后认知功能障碍和谵妄的一个原因。然而，没有合适的药物可用于治疗神经认知性皮炎。本研究评估了用七氟烷麻醉预处理对脂多糖（LPS）诱导的系统性炎症的动物模型中的认知和神经炎症变化导致的可能的神经保护作用。
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方法：成年小鼠随机分为（1）对照组，（2）2%七氟烷预处理1h, (3)腹腔注射LPS 5mg/kg，(4)2﹪七氟烷预处理1h+LPS注射组。再注射5mg/kg LPS后24小时，使用免疫染色和免疫印迹测定海马中小胶质细胞标记物离子钙接头蛋白抗体(Iba-1)。采用1L-1β和1L-6作为免疫印迹法的炎症标记物，并进行淀粉样蛋白前体蛋白裂解酶1（BACE1）免疫印迹的β位以评估淀粉样蛋白β-蛋白（Αβ）积聚。长期认知功能障碍评估使用恐惧条件测试。
结果：腹腔内LPS增加了Iba-1（150％），炎症标志物（160％）和Αβ积聚物（350％）的水平，并且七氟烷预处理抑制了这些增加。全身LPS导致学习障碍。七氟烷还维持接受LPS注射小鼠的长期记忆。七氟烷预处理通过减少过度小胶质细胞活化，炎症和Αβ积聚来预防全身LPS小鼠模型所致的长期记忆障碍。
结论：本研究支持七氟烷预处理可能对神经元炎症有益的假说。七氟烷可能对减少术后认知功能障碍和谵妄有益。
Maiko Satomoto1,2)*, Zhongliang Sun1)*, Yushi U. Adachi1),Hiroyuki Kinoshita3), and Koshi Makita1) Sevoflurane preconditioning ameliorates lipopolysaccharide-induced cognitive impairment in mice.
BACKGROUND:Systemic inflammation induces brain neuronal inflammation, in turn causing acute cognitive disorders. Furthermore, neuronal inflammation is one cause of postoperative cognitive disorder (POCD) and delirium. However, no sufficiently established pharmacological treatment is available for neurocognitive inflammation. This study evaluated the possible neuroprotective effects of preconditioning with sevoflurane anesthesia on cognition and neuroinflammatory changes in an animal model of lipopolysaccharide (LPS)-induced systemic inflammation
METHODS:Adult mice were randomly divided into (1) control, (2) 2% sevoflurane preconditioning for 1 h, (3) intraperitoneal 5 mg/kg LPS injection, and (4) 2% sevoflurane preconditioning for 1 h + LPS injection groups. At 24 h after 5 mg/kg LPS injection, microglial activation based on ionized calcium-binding adapter molecule 1 (Iba-1) expression in the hippocampus was determined using immunostaining and immunoblotting. IL-1β and IL-6 immunoblotting were used as inflammation markers, and β-site of amyloid precursor protein cleaving enzyme 1 (BACE1) immunoblotting was performed to evaluate amyloid β-protein (Aβ) accumulation. Long-term cognitive impairment was evaluated using fear conditioning tests.
RESULTS:Intraperitoneal LPS increased levels of Iba-1 (150%), inflammation markers (160%), and Aβ accumulation (350%), and sevoflurane preconditioning suppressed these increases. Systemic LPS caused learning deficits. Sevoflurane also maintained long-term memory in mice receiving LPS injection. Sevoflurane preconditioning prevented long-term memory impairment in the mouse model administered systemic LPS by decreasing excessive microglial activation, inflammation, and Aβ accumulation.
CONCLUSIONS:This study supports the hypothesis that sevoflurane preconditioning might also be beneficial for neuronal inflammation. Sevoflurane might be beneficial for reducing delirium and POCD.
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