Anesthetic Propofol Attenuates Apoptosis, Aβ Accumulation, and Inflammation Induced by Sevoflurane Through NF-κB Pathway in Human Neuroglioma Cells

Abstract

Anesthetics have been reported to promote Alzheimer's disease neuropathogenesis by inducing amyloid beta (Aβ) protein accumulation and apoptosis. The aim of this study was to evaluate the effect of propofol on the apoptosis, Aβ 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 Aβ 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-κB) was tested by Western blot and immunofluorescence assay. We found that the activation of NF-κB pathway was suppressed by propofol. The results suggest that propofol can effectively attenuate the apoptosis, Aβ accumulation, and inflammation induced by sevoflurane in human neuroglioma cells through NF-κB signal pathway.

Propofol attenuates intermittent hypoxia induced up-regulation of proinflammatory cytokines in microglia through inhibiting the activation of NF-Bκ/p38 MAPK signalling

“…Recently, the anti-inflammatory property of propofol has attracted increasing attention. A wealth of information linking that propofol prohibited inflammatory response through preventing the NF-κB and p38 MAPK signalling and then reducing the release of inflammatory mediators is published [25,26]. In addition, emerging evidence showed that propofol selectively attenuated the activation of NF-κB and p38 MAPK in vascular endothelium during IH exposure [16].…”

“…Propofol blocked astrocyte activation upon stimulation with LPS via presenting the NF-κB, p38 MAPK and extracellular signal-regulated protein kinases (ERK) 1/2 pathways [33]. Moreover, propofol exerted effectively anti-inflammatory properties in human neuroglioma cells treated by sevoflurane through suppressing the NF-κB signalling pathway [26]. An earlier report supported that anti-inflammatory mechanisms of propofol were shown through decreasing the level of phosphorylated p38 MAPK [25].…”

“…And it attenuated secretion of proinflammatory cytokines in a hepatocyte nuclear factor-1α-dependent manner [19]. Emerg ing reports suggested that propofol effectively down-regulated inflammatory responses by inhibiting the phosphorylation of nuclear factor-κB (NF-κB) and p38 mitogen-activated protein kinase (MAPK) [25,26,33]. Propofol blocked astrocyte activation upon stimulation with LPS via presenting the NF-κB, p38 MAPK and extracellular signal-regulated protein kinases (ERK) 1/2 pathways [33].…”

Cognitive decline in the elderly after surgery and anaesthesia: results from the Oxford Project to Investigate Memory and Ageing (OPTIMA) cohort

“…Cell and animal studies have gone some way in showing some potentially damaging effects of certain anaesthetics, for example, inhalational anaesthetics such as isoflurane and sevoflurane 5, 6, 7, 8, 9, 10. In contrast, the intravenous anaesthetic, propofol, may have largely protective effects 6, 11, 12, 13, mainly shown in animal and cellular models, although it has also been suggested to have some negative actions 14.…”

Impact of propofol on renal ischemia/reperfusion endoplasmic reticulum stress

“…Hence, it is particularly important to have measures that can promptly prevent this type of injury. Studies have found that intravenous anesthetic propofol (Pro) shows properties such as antioxidation, antiinflammation, and anti-apoptosis 3,4 , and could reduce I/R injury in organs including the liver, kidney, and brain [5][6][7] ; however, its effects on the signals of the endoplasmic reticulum stress apoptosis pathway, during renal I/R injury, are yet to be reported. In this study, we observed the effects of Pro on the expressions of CHOP and caspase-12 in renal I/R injury, aiming to explore the molecular mechanisms related to the actions of Pro in renal I/R injury prevention.…”