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. 2015 Jun 10;10(6):e0129693. doi: 10.1371/journal.pone.0129693

Fig 7. PI3-kinase-dependent propofol treatment reduces MTP loss and caspase-3 activation in primary neutrophils and ATRA-differentiated granulocytic HL60 cells.

Fig 7

(A) Isolated human primary neutrophils and (B) ATRA (1 μM)-differentiated granulocytic HL60 cells were treated with propofol with or without LY294002 treatment for the indicated time points. A rhodamine 123-based flow cytometric analysis and caspase-3 activity assay were used to detect MTP loss (% of positive cells) and caspase-3 (OD) activation, respectively. The data are shown as the means ± SD of three individual experiments. *P < 0.05 and **P < 0.01 compared with untreated at 0 h. #P < 0.05 compared with untreated at 24 h or day 6. †P < 0.05 compared with propofol. (C) A hypothetic signaling model of propofol-mediated cytoprotection in the constitutive apoptosis of neutrophils. Through an unknown mechanism, treatment of non-toxic dose of propofol may reverse downregulation of PI3-kinase, AKT, Mcl-1, and MTP, and activation of GSK-3β and caspase-3 in neutrophils under constitutive apoptosis.