Abstract:  Objective    To explore the therapeutic effect and mechanism of Klotho protein on POCD by selecting the POCD aged rats and BV2 microglia as research objects.    Methods    Forty-five SD aged rats were divided into a control group, a sevo group and a sevo+surgery group, randomly. The rats cognitive status were assessed by water maze. HE staining, TUNEL staining and ELISA were used to detect the pathological changes, apoptosis and expression levels of inflammatory factors in rat hippocampus. Western blot was used to detect the related proteins expression of the rat hippocampal tissue and BV2 cells. Cell immunofluorescence was used to detect the NF-κB p65 expression in BV2 cells.    Results    Aged rats in the sevo and sevo+surgery groups showed significant cognitive impairment, hippocampal region damage, increased expression of inflammatory factors, apoptosis of a large number of neuronal cells, down-regulation of Klotho protein expression, and up-regulation of FGF23/NF-κB pathway protein expression. LPS and sevoflurane induced increased expression of inflammatory factors and up-regulated expression of FGF23/NF-κB pathway protein in BV2 cells, while treatment with Klotho decreased the expression levels of inflammatory factors and the above proteins.    Conclusions    Klotho may become a new target in the prevention and treatment of POCD, and its mechanism may be related to the inhibition of FGF23/NF-κB expression in microglia by Klotho peotein.

Key words: Sevoflurane; ,  Postoperative cognitive dysfunction; ,  Klotho; ,  Microglia; ,  FGF23; ,  NF-κB