Fig. 7
From: Placenta-derived IL-32β activates neutrophils to promote preeclampsia development
IL-32β activates PMNs mainly by binding to PR3. The PR3 inhibitor α1-antitrypsin inhibited the IL-32β-induced production of ROS (a) and surface expression of CD11b (b) and CD66b (c) in PMNs in a dose-dependent manner. d The αVβ3 integrin inhibitor Echistatin, α1 isoform did not inhibit IL-32β-induced ROS production. A high concentration of Echistatin, α1 isoform slightly inhibited the IL-32β-induced surface expression of CD11b (e) and CD66b (f) on PMNs. g The expression levels of gp91phox, p47phox, TNFα, and IL-1β in PMNs pretreated with 400 nM Echistatin, α1 isoform or 0.4 mg·mL−1 α1-antitrypsin. The results are from four independent experiments. The data were analyzed by two-way ANOVA with Tukey’s multiple comparisons test. Error bars, mean + SD. *P < 0.05; **P < 0.01; ***P < 0.001, IL-32β compared with the corresponding Ctrl. #P < 0.05; ##P < 0.01; ###P < 0.001 versus vehicle in the IL-32β-treated group
