Anesthetic Propofol Attenuates Apoptosis, A beta Accumulation, and Inflammation Induced by Sevoflurane Through NF-kappa B Pathway in Human Neuroglioma Cells

Anesthetics have been reported to promote Alzheimer's disease neuropathogenesis by inducing amyloid beta (A beta) protein accumulation and apoptosis. The aim of this study was to evaluate the effect of propofol on the apoptosis, A beta accumulation, and inflammation induced by sevoflurane in human neuroglioma cells. Human neuroglioma cells were treated with or without sevoflurane and then co-incubated with or without propofol. Cell apoptosis was evaluated by fluorescence-activated cell sorting analysis (FACS) using AV-PI kits, and data showed that apoptosis induced by sevoflurane was significantly attenuated by propofol treatment. In addition, with the reactive oxygen species (ROS) production measured by FACS after staining with dichloro-dihydrofluorescein diacetate, propofol could significantly reduce the production of ROS as well as the accumulation of A beta induced by sevoflurane assessed by enzyme-linked immuno sorbent assay (ELISA) analysis. On the other hand, the same treatment decreased the inflammation factor production of interleukin-6. Moreover, the level of nuclear factor-kappa B (NF-kappa B) was tested by Western blot and immunofluorescence assay. We found that the activation of NF-kappa B pathway was suppressed by propofol. The results suggest that propofol can effectively attenuate the apoptosis, A beta accumulation, and inflammation induced by sevoflurane in human neuroglioma cells through NF-kappa B signal pathway.