Fig. 1: Cardiolipin (CL) alteration in the injured spinal cord following spinal cord injury (SCI).

A–C Biomarkers of apoptosis following SCI. Time course of cytochrome c release (A), Smac/DIABLO release (B), and active caspase-3 expression (C) following SCI. *P < 0.05, **P < 0.01 vs sham (One-way ANOVA, Dunnett post-test, n = 4 rats/group). Data represent mean ± s.e.m. Cyt. c cytochrome c, Smac/D. Smac/DIABLO, A. casp.-3 active casepase-3. D–I Lipidomic analysis after SCI. Lipid extracts of spinal cord from sham, 3 h, and 24 h SCI rats were prepared by using the methyl-tert-butyl ether (MTBE) extraction. D, E Expanded negative-ion ESI mass spectra of rat spinal cord lipid extracts obtained using a Q Exactive™ Hybrid Quadrupole-Orbitrap mass spectrometer. The asterisks indicate the identified CL plus-one isotopologues, which were characteristic of the doubly charged CL molecular species and were used to quantify individual CL molecular species. Each spectrum is displayed after being normalized to the intensity of internal standard 1’, 3’-bis [1, 2-dimyristoyl-sn-glycero-3-phospho]-sn-glycerol (tetra14:0 CL, [CL-2H + 1]^2- = 619.91791) ion. The x-axis is mass-to-charge ratio (m/z). A significant decrease in CL was detected at 3 and 24 h post-injury (D–F) while a corresponding increase in lyso-CL and ratio of lyso-CL/CL was observed at 24 h post-injury (G, H). 4-HNE, a marker of lipid peroxidation, was significantly increased at 3 and 24 h after SCI (I). Data represent mean ± s.e.m. *P < 0.05, **P < 0.01 (One-way ANOVA, Tukey’s multiple comparisons test, n = 4 rats/groups). CL cardiolipin, Lyso-CL lyso-cardiolipin, 4-HNE 4-hydroxy Nonenal.