Fig. 2: Amitriptyline induces cerebral endothelial intracellular ROS production in normoxia and post-I/R. | Cell Death & Disease

Fig. 2: Amitriptyline induces cerebral endothelial intracellular ROS production in normoxia and post-I/R.

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. 2: Amitriptyline induces cerebral endothelial intracellular ROS production in normoxia and post-I/R.

Oxidative stress, determined by A the intracellular ROS detection agent CellROX®, a green fluorescent indicator, or B the mitochondria-selective ROS detection agent MitoSOX®, a red fluorescent indicator, of cerebral microvascular endothelial hCMEC/D3 exposed to Nx (21% O2) or OGD (1% O2) for 24 h followed by 3 h of reoxygenation (Reox) in full medium for 24 h (OGD/R), which were treated with control medium (Ctrl) or amitriptyline (Ami; 50 µM) during Reox. C Lipid peroxidation, evaluated by thiobarbituric acid reactive substances (TBARS) formation, of ischemic brain tissue samples and plasma samples of mice exposed to intraluminal middle cerebral artery occlusion (MCAO), which were i.p. treated with vehicle or the ASM inhibitors Ami (12 mg/kg) or fluoxetine (10 mg/kg) starting immediately after reperfusion. Mice were sacrificed 24 h post-MCAO. Samples were analyzed by ImageJ software. Representative samples are depicted. Data are mean ± SD values. Evaluated by one-way ANOVA followed by Bonferroni (A, B) or LSD (C) tests. *p ≤ 0.05/**p ≤ 0.01/***p ≤ 0.001 (A n = 6; B n = 4; and C n = 5–6 independent samples/group).

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