前言
术后认知功能障碍是一种常见的术后并发症，随着患者年龄的增长发生率也不断提高。不仅不利于患者康复，增加并发症发生率，而且增加医疗费用支出和患者家庭负担。但其确切的发病原因和机制都尚不明确，还需要进一步探索，为临床防治提供确切的帮助。神经炎症被认为是POCD的机制之一，有效抑制神经炎症的发生是否可以减轻甚至防止POCD的发生呢？且看看下面这篇文献的结果吧！
Histone Deacetylase Inhibitor MS-275 Alleviates Postoperative Cognitive Dysfunction in Rats by Inhibiting Hippocampal Neuroinflammation.
Neuroinflammation in the hippocampus plays essential roles in postoperative cognitive dysfunction (POCD). Histone deacetylases (HDACs) have recently been identified as key regulators of neuroinflammation. MS-275, an inhibitor of HDAC, has been reported to have neuroprotective effects. Therefore, the present study aimed to test the hypothesis that pretreatment with MS-275 prevents POCD by inhibiting neuroinflammation in rats. In this study, anesthesia/surgery impaired cognition, demonstrated by an increase escape latency and reduction in the number of platform crossings in Morris water maze (MWM) trials, through activating microglia neuroinflammation and decreasing PSD-95 expression. However, pretreatment with MS-275 attenuated postoperative cognitive impairment severity. Furthermore, pretreatment with MS-275 decreased activated microglia levels and increased PSD95 protein expression in the hippocampus. Pretreatment with MS-275 reduced NF-κB-p65 protein expression and nuclear accumulation as well as the neuroinflammatory response (production of proinflammatory cytokines including TNF-α and IL-1β) in the hippocampus. Additionally, MS-275 reduced HDAC2 expression and HDAC activity in the hippocampus, which were enhanced in vehicle-treated rats. These results suggest that MS-275 alleviates postoperative cognitive dysfunction by reducing neuroinflammation in the hippocampus of rats via HDAC inhibition
组蛋白去乙酰化酶*制剂抑**MS-275通过抑制海马神经炎症减轻大鼠术后认知功能障碍。
海马中的神经炎症在术后认知功能障碍（POCD）中起重要作用。最近组蛋白去乙酰化酶（HDACs）被确定为神经炎症的关键调节因子。据报道，MS-275是一种HDAC*制剂抑**，具有神经保护作用。因此，本研究旨在检验假设：MS-275预处理通过抑制大鼠神经炎症来预防POCD。在这项研究中，麻醉/手术通过激活小胶质细胞神经炎症和降低PSD-95表达损害认知功能，Morris水迷宫（MWM）试验中逃避潜伏期增加和穿过平台次数减少。然而，MS-275预处理减轻了术后认知障碍的严重程度。此外，用MS-275预处理降低了激活的小胶质细胞水平并增加了海马中PSD95蛋白的表达。用MS-275预处理减少了海马中NF-κB-p65蛋白的表达和其在细胞核内的沉积以及神经炎症反应（包括TNF-α和IL-1β的促炎细胞因子的产生）。另外，MS-275降低了海马中的HDAC2表达和HDAC活性，其在载体转染大鼠中增强。这些结果表明MS-275通过抑制HDAC减少大鼠海马神经炎症，从而减轻术后认知功能障碍