Sevoflurane-Mediated Activation of p38-Mitogen-Activated Stresskinase is Independent of Apoptosis in Jurkat T-Cells

Abstract

Sevoflurane is a specific activator of the apoptosis signal-regulating kinase-1-, MKK3/MKK6-p38 MAP kinase cascade in Jurkat T-cells. Our data suggest that sevoflurane-induced p38 activation is not affected by caspase activation. Furthermore, sevoflurane-induced apoptosis is not dependent on p38 MAP kinase activation.

Sevoflurane inhibits invasion and migration of lung cancer cells by inactivating the p38 MAPK signaling pathway

“…Our results are not consistent with their results, possibly due to our use of a different category of cell line (Loop and Roesslein [14,15] used human T lymphocytes and Jurkat T-cells). However, the cell line investigated in this study is a human lung adenocarcinoma A549 cell line.…”

“…Loop and Roesslein [14,15] found that sevoflurane activates the p38 MAPK signaling pathway and increases phosphorylation of p38 MAPK. Our results are not consistent with their results, possibly due to our use of a different category of cell line (Loop and Roesslein [14,15] used human T lymphocytes and Jurkat T-cells).…”

“…Protocol of A549 cell exposure to sevoflurane A549 cells in the exponential growth phase were inoculated onto plates and cultured in a CO 2 incubator (ThermoFisher Scientific, Waltham, MA) for 24 h. In accordance with the experimental protocol previously described [14,15], cell culture plates were placed in an airtight glass chamber with inlet and outlet connectors. The inlet port of the chamber was connected to the anesthesia machine (Cicero-EM 8060; Dräger, Germany), and sevoflurane was supplied into the chamber by a sevoflurane vaporizer (Sevorane; Abbott, Abbot Park, IL) attached to the anesthesia machine.…”

Attenuating sevoflurane-induced cellular injury of human peripheral lymphocytes by propofol in a concentration-dependent manner

“…In the sevoflurane group, the cells were put in a 1.2 L sealed container, which was connected to an anaesthesia apparatus (Dräger Fabius GS) that had a sevoflurane vapor (Dräger Vapor 2000), and could consistently supply 8% sevoflurane, air and 5% CO 2 . The container was placed into a 5% CO 2 incubator, and the cells were cultured for 24 h at 37 o C. The concentration and duration of sevoflurane administration were selected based on our preliminary experiments and previous reports (Matsuoka et al, 2001;Loop et al, 2005;Roesslein et al, 2008). In the propofol + sevoflurane groups, the cells were cultured in RPMI 1640 media containing propofol at concentrations of 5, 10, 25 or 50 µg/mL, and 15 min later the cells were exposed to 8% sevoflurane as above for 24 h at 37 o C in a 5% CO 2 incubator.…”

“…Sevoflurane induces apoptosis in various types of human cells including peripheral polymorphonuclear neutrophils (Wong et al, 2006), primary T lymphocytes (Loop et al, 2005), Jurkat T cells (Loop et al, 2005;Roesslein et al, 2008), and other cells (Kvolik et al, 2005). Its pro-apoptotic activity can be explained by its ability to increase disruption of the mitochondrial membrane (which reduces the membrane potential, ∆Ψm), activate caspase-3, and release cytochrome c (Loop et al, 2005), or to trigger the formation of peroxynitrite and increase production of reactive oxygen species (ROS) (Wong et al, 2006), or to mediate activation of p38-mitogen-activated protein kinase cascades (Roesslein et al, 2008).…”