抗衰老蛋白Klotho通过降低NF-κBp65 活性抑制炎性介质的释放，但其在POCD的作用机制尚未清楚。前期研究发现klotho与氧化应激诱导的POCD密切相关，且Klotho显著抑制巨噬细胞聚集，改善POCD。klotho 可能通过PKC/PDLIM2/NF-κB和FGF23/NF-κB信号通路调节巨噬细胞侵润，拮抗POCD的发展。为此，本课题拟利用klotho过表达和沉默的腺病毒，在POCD大鼠模型和巨噬细胞RAW264.7中，klotho改善POCD的作用，揭示klotho调节PKC/PDLIM2/NF-κB和FGF23/NF-κB信号通路，抑制巨噬细胞侵润的分子机制，为POCD的防治提供理论依据。

The major invasion of macrophages mediated by NF- kappa Bp65 activation is the main cause of postoperative cognitive dysfunction (POCD). Anti senescence protein Klotho inhibits the release of inflammatory mediators by reducing the activity of NF- kappa Bp65, but its mechanism of action in POCD has not been elucidated. Our previous study found that Klotho was closely related to POCD induced by oxidative stress, and Klotho significantly inhibited macrophage aggregation and improved POCD. It is suggested that Klotho may regulate the invasion of macrophages through the PKC/PDLIM2/NF- kappa B and FGF23/NF- kappa B signaling pathway and antagonize the development of POCD. Therefore, this project intends to use the Klotho adenovirus expression and silence, in the rat model of POCD and RAW264.7 in Klotho macrophages, clarify the function of improving POCD, PKC/PDLIM2/NF- and B indicated that Klotho regulates FGF23/NF- kappa B signaling pathway, molecular mechanism of inhibition of macrophage infiltration, provide theoretical and experimental basis for the prevention and treatment of POCD.