PQ delayed neutrophil apoptosis in a concentration-independent manner.

<p>Neutrophil apoptosis was assessed with annexin V-FITC and PI staining followed by flow cytometry. Compared with the control, the doses of PQ (5, 50, or 100 μM) significantly attenuated neutrophil apoptosis at all time points after treatment (6, 12, 18, and 24 h). No difference was found between different concentration groups. *<i>P</i><0.05 compared with control at the same time point.</p

Algorithm of HDBN.

<p>Algorithm of HDBN.</p

Architecture of CRBM.

<p>Architecture of CRBM.</p

TNF-α and IL-6, but not IL-1β, formed a positive-feedback circuit with ROS generation upon PQ stimulus.

<p>(A) TNF-α, IL-1β, and IL-6 production levels were remarkably promoted by PQ and significantly decreased by DPI. (B) PQ-induced ROS generation was decreased by preincubation with TNF-α or IL-6 antibody respectively, but not by IL-1β, which indicated a positive-feedback circuit between the regulation of ROS generation and TNF-α and IL-6 production under PQ stimulus. ROS contents were normalized to control. *<i>P</i><0.05.</p

Algorithm of AHD.

<p>Algorithm of AHD.</p

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ROS were involved in PQ-induced neutrophil apoptosis delay.

<p>(A) ROS generation was assessed with DCFH-DA fluorescence intensity and was remarkably increased by all PQ concentration (5, 50, and 100 μM) at all time points (6, 12, 18, and 24 h) in a concentration-independent manner. (B) DPI or apocynin pretreatment suppressed PQ-induced ROS generation. (C) PQ-induced neutrophil apoptosis was also attenuated by DPI or apocynin pretreatment. ROS contents were normalized to control. *<i>P</i><0.05.</p

p38 MAPK and NF-κB signaling pathways, but not Akt, were involved in PQ-induced ROS generation and reduced neutrophil apoptosis.

<p>(A, B) p-p38 MAPK and p-Mcl-1 production were predominantly induced by PQ and suppressed by DPI co-treatment. The specific p38 MAPK inhibitor SB203580 blocked both p-p38MAPK and p-Mcl-1 productions, whereas SC200137 suppressed p-Mcl-1 but not p-p38MAPK. (C) The Akt pathway was not affected by PQ. (D, E) Both p-IκBα and p-P65 were activated by PQ pretreatment and decreased by DPI. (F) PQ-mediated reduction in neutrophil apoptosis could be rescued by SB203580, SC200137, and PDTC but not SC221226, which indicated that p38MAPK, Mcl-1, and NF-κB pathways were involved in the PQ-regulated decrease in neutrophil apoptosis. *<i>P</i><0.05.</p

Architecture of HDBN.

<p>Architecture of HDBN.</p

Analytical HPLC analysis of purified antisense oligonucleotide.

<p>Sample preparation: 25 µL purified antisense oligonucleotide; Column: DNAPac PA-100 (4/250); Flow rate: 1 ml/min; Buffer A: 10 mM NaClO₄+1 mM Tris; Buffer B: 300 mM NaClO₄+1 mM Tris; Gradient: 10–70% B, 7.6 CV.</p