Fig. 1: Spermine triggers inflammatory cell death and activates necroptotic molecules.
From: Ferroptosis-activating metabolite acrolein antagonizes necroptosis and anti-cancer therapeutics
A Real-time analysis of cell death in bone marrow-derived macrophages (BMDMs) treated with different doses of spermine (Spm). B Representative images of cell death in BMDMs at 0 and 12 h of indicated doses of Spm treatment. C, D Immunoblot analysis of (C) released lactate dehydrogenase (LDH) and high mobility group box 1 (HMGB1) in the cell culture media; (D) phosphorylated receptor-interacting serine/threonine kinase 3 (pRIPK3), total RIPK3 (tRIPK3), phosphorylated mixed lineage kinase domain-like pseudokinase (pMLKL), and total MLKL (tMLKL) after indicated times of Spm treatment. GAPDH was used as internal control. E, F Immunoblot analysis of (E) pRIPK3, tRIPK3, pMLKL, and tMLKL; (F) released LDH and HMGB1 in the cell culture media in BMDMs after indicated doses of Spm treatment. β-actin was used as an internal control (E). G Real-time analysis of cell death in BMDMs treated with Spm in the presence or absence of necrostatin-1 (Nec-1). H Immunoblot analysis of released LDH and HMGB1 in the cell culture media after indicated treatments in BMDMs. Data are shown as mean ± SEM; ****P < 0.0001 (two-way ANOVA; n = 4 from 4 biologically independent samples) (A and G). Data are representative of at least three independent experiments (B–F and H). Scale bar, 100 μm (B). Source data are provided as a Source Data file.
