Figure 9.
Figure 9. The effect of NBD on LPS-, GM-CSF–, DEX-, and IL-8–delayed apoptosis. Cells were incubated with buffer control (▪), 10 μM TAT-NBD (□), or the same concentration of a mutant control peptide (▦) in the absence or presence of 100 ng/mL LPS (A), 20 ng/mL GM-CSF (B), 10–7 M DEX (C), or 100 nM IL-8 (D). After 20 hours cells were harvested and the percentage of apoptotic PMNs was assayed by flow cytometry using annexin V staining (n = 5 for LPS, GM-CSF, DEX; n = 4 for IL-8). The data indicate that LPS did not inhibit apoptosis in the presence of TAT-NBD, whereas significant delay of apoptosis occurred in the presence of buffer control or the mutant control peptide. Although TAT-NBD had no effect on the delayed apoptosis by DEX and IL-8, TAT-NBD prevented delayed apoptosis by GM-CSF (**P < .01 when compared to untreated cells).

The effect of NBD on LPS-, GM-CSF–, DEX-, and IL-8–delayed apoptosis. Cells were incubated with buffer control (▪), 10 μM TAT-NBD (□), or the same concentration of a mutant control peptide (▦) in the absence or presence of 100 ng/mL LPS (A), 20 ng/mL GM-CSF (B), 10–7 M DEX (C), or 100 nM IL-8 (D). After 20 hours cells were harvested and the percentage of apoptotic PMNs was assayed by flow cytometry using annexin V staining (n = 5 for LPS, GM-CSF, DEX; n = 4 for IL-8). The data indicate that LPS did not inhibit apoptosis in the presence of TAT-NBD, whereas significant delay of apoptosis occurred in the presence of buffer control or the mutant control peptide. Although TAT-NBD had no effect on the delayed apoptosis by DEX and IL-8, TAT-NBD prevented delayed apoptosis by GM-CSF (**P < .01 when compared to untreated cells).

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