Sevoflurane But Not Propofol Provided Dual Effects of Cell Survival in Human Neuroblastoma SH-SY5Y Cells

Abstract

Background: We have hypothesized that the most commonly used intravenous (propofol) and inhalational (sevoflurane) general anesthetics affect cell survival concentration and duration dependently with different potency associated with their differential potency to affect intracellular calcium homeostasis. Methods: Human neuroblastoma SH-SY5Y cells stably transfected with either wild type or M146L mutant human presenilin 1 were cultured and exposed to equipotent of propofol or sevoflurane. Cell viability, cytosolic and mitochondrial calcium were measured. Results: Sevoflurane but not propofol, at clinically relevant concentrations and durations, promoted cell survival. Prolonged exposure (24 hours) of 1% sevoflurane resulted in significant cell damage in both types of cells. Both sevoflurane and propofol had significantly higher cell response rates to the elevation of cytosolic calcium or mitochondrial calcium in the presence of extracellular calcium. With the contribution of calcium influx, sevoflurane but not equipotent 1 MAC propofol, caused a significantly greater increase in peak and overall calcium in Alzheimer’s mutation cell than in wild type cells, but significantly more increase in overall mitochondrial calcium concentrations in wild type than mutation cells. In the absence of extracellular calcium influx, sevoflurane, but not propofol, caused more significant elevations of overall mitochondrial calcium concentration in mutation cells than control cells. Conclusion: Calcium influx contributed to the general anesthetics mediated elevation of cytosolic or mitochondrial calcium, which is especially true for propofol. Sevoflurane has a greater potency to either promote or inhibit cell survival than propofol, which may be associated with its ability to affect cytosolic or mitochondrial calcium.

Sevoflurane inhibits neuroblastoma cell proliferation and invasion and induces apoptosis by miR‐144‐3p/YAP1 axis

“…Also, Müller‐Edenborn et al 30 found that SEV slows down colon cancer progression in vitro by inhibiting MMP9. Recently, Gao et al 31 found that SEV (but not propofol) promoted the survival of human NB SH‐SY5Y cells at clinically relevant concentrations and durations. However, 1% SEV caused significant cell damage after its prolonged exposure (24 h) 31 .…”

“…Recently, Gao et al 31 found that SEV (but not propofol) promoted the survival of human NB SH‐SY5Y cells at clinically relevant concentrations and durations. However, 1% SEV caused significant cell damage after its prolonged exposure (24 h) 31 . We hypothesized that SEV also repressed NB in view of its inhibitory properties in various tumour cells.…”

“…29 Also, Müller-Edenborn et al 30 found that SEV slows down colon cancer progression in vitro by inhibiting MMP9. Recently, Gao et al 31 found that SEV (but not propofol) promoted the survival of human NB SH-SY5Y However, 1% SEV caused significant cell damage after its prolonged exposure (24 h). 31 We hypothesized that SEV also repressed NB in view of its inhibitory properties in various tumour cells.…”

“…Recently, Gao et al 31 found that SEV (but not propofol) promoted the survival of human NB SH-SY5Y However, 1% SEV caused significant cell damage after its prolonged exposure (24 h). 31 We hypothesized that SEV also repressed NB in view of its inhibitory properties in various tumour cells. Fortunately, our data revealed that SEV abates NB cell proliferation and invasion and induces apoptosis dose-dependently, which further confirmed our hypothesis.…”