术后认知功能障碍（POCD）不仅影响术后病人的康复，严重者会导致痴呆，危害巨大，但发病机理尚不清楚。我们前期临床研究证实较深丙泊酚麻醉可减少POCD发生率，有研究也表明丙泊酚在体外能够抑制低氧或脂多糖等诱导的小胶质细胞激活。在此基础上，我们拟进行如下研究：1.在不同深度丙泊酚麻醉下行大鼠肝乳头叶切除，观察中枢神经系统炎症变化及其和神经元凋亡与再生、突触可塑性以及认知功能变化之间的关系；2. 阐明不同浓度丙泊酚对原代小胶质细胞激活的影响及其分子机制；3. 在体利用转基因技术特异性清除小胶质细胞，观察丙泊酚不同深度麻醉下对神经细胞凋亡和再生以及认知功能的影响，并在体验证细胞水平得到的分子机制。本研究通过体外和在体模型，利用细胞、分子生物学和神经行为学等技术手段，系统深入研究深麻醉改善POCD的神经炎症机制，旨在为临床POCD的防治提供实。

Postoperative cognitive dysfunction (POCD) is a well-recognised complication after surgery, but evidence of POCD has been lacking. It affects both the patients' prognosis and postoperative life quality; furthermore, it also can lead to dementia. Our previous study showed that deeper total intravenous anesthesia could reduce the incidence of POCD. Other studies have shown that propofol could restrain the activation of microglia induced by hypoxia or lipopolysaccharide. On this basis, we intend to carry out the following study:.1. To investigate the changes of inflamatory in the central nervous system,neuronal apoptosis and regeneration,synaptic plasticity and cognitive function under different depth of anesthesia during resection of hepatic papilla;.2. To investigate the molecular mechanisms of different concentrationpropofol restraining the activation of primary microglia;.3. To investigate different depth of propofol anesthesia onneuronal apoptosis and regeneration,synaptic plasticity and cognitive function under transgenic technology to remove microglia specially..We schedule to thoroughly study the mechanism of deeper anesthesia alleviate neuroinflammation by means of cell biology,molecular biology and neuroethology.