Fig. 3: Plasmodium berghei ANKA-infected red blood cells activate caspases, induce apoptosis, and promote increased permeability in DBA/2 mice pulmonary endothelial cells.
From: Blockade of caspase cascade overcomes malaria-associated acute respiratory distress syndrome in mice
PMLECs from naive DBA/2 mice were stimulated with Plasmodium berghei ANKA-infected red blood cells (PbA-iRBCs) or non-infected red blood cells (RBC). A Representative images of apoptotic cells (with brown nuclei) stained by TUNEL assay and counterstained with Harris Hematoxylin (blue). B Quantification of death cells was analyzed in 15 fields per slide with ×200 magnification. C–F Enzymatic activity of caspases quantification. Data expressed as mean ± SE; Kruskal–Wallis test, followed by Dunn’s post test, where###p < 0.001 with respect to the positive control (PC), $$$p < 0.001 with respect to NE and ***p < 0.01 with respect to PbA-iRBC. G PMLECs were also treated with 50 μM of ZVAD-fmk (caspase inhibitor) for 24 h and compared to NS to evaluate the permeability using Evans blue in a Transwell assay. B–F Data analyzed from two grouped experiments and expressed as mean ± SE; Kruskal–Wallis test, followed Dunn test (n = 7–10 wells/group; *p < 0.05, **p < 0.01, and ***p < 0.001). G ANOVA, followed Tukey multiple comparison test. NS: non-stimulated; iRBC: Plasmodium berghei ANKA-infected red blood cells; RBC: non-infected red blood cells; Zvad: ZVAD-fmk (caspase inhibitor) treatment.
