Fig. 4: Amitriptyline reduces cerebral endothelial proliferation in normoxia and post-I/R without influencing cell survival. | Cell Death & Disease

Fig. 4: Amitriptyline reduces cerebral endothelial proliferation in normoxia and post-I/R without influencing cell survival.

From: Acid sphingomyelinase inhibition induces cerebral angiogenesis post-ischemia/reperfusion in an oxidative stress-dependent way and promotes endothelial survival by regulating mitochondrial metabolism

Fig. 4: Amitriptyline reduces cerebral endothelial proliferation in normoxia and post-I/R without influencing cell survival.

A, B Proliferation of cerebral microvascular endothelial hCMEC/D3 cells exposed to Nx (21% O2; in A) or OGD (1% O2) for 24 h followed by reoxygenation (Reox) for 48 h in full medium (OGD/R; in B), evaluated by Coomassie blue staining, after treatment with control medium (Ctrl), phorbol-12-myristate-13-acetate (PMA; 1 µM) or amitriptyline (Ami; 10–50 µM). C, D Cell viability, assessed by the 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay, of hCMEC/D3 cells exposed to Nx (21% O2) or OGD (1% O2) for 24 h followed by Reox for 24 h. Cells were treated with Ctrl or Ami (50 µM; in C) or Ctrl, Ami (50 µM) or Luperox® (0.1 µM or 1 µM; in D). Plates were scanned and analyzed using ImageJ software. Data were processed as triplicates, of which mean values were formed. Results of 3 independent experiments are presented. Data are mean ± SD values. Evaluated by one-way or two-way ANOVA, as adequate, followed by Bonferroni tests. *p ≤ 0.05/**p ≤ 0.01 compared with corresponding Ctrl.

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