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. Author manuscript; available in PMC: 2010 Jun 7.
Published in final edited form as: J Neurochem. 2006 Apr 21;97(5):1301–1313. doi: 10.1111/j.1471-4159.2006.03797.x

Fig. 2.

Fig. 2

15-A2t-Isoprostane (15-A2t-IsoP) induces apoptotic neuronal death. (a, b) 4′-6-Diamidino-2-phenylindole (DAPI) staining of neurons treated with vehicle (a) or 30 μM 15-A2t-IsoP for 24 h (b) demonstrates an increase in asymmetric chromatin formations (arrows), an indication of apoptosis. (c, d) Neuronal culture treated for 48 h with vehicle (c) vs. 30 μM 15-A2t-IsoP (d). IsoP-treated cells (d) show a loss of microtubule-associated protein 2 (MAP-2) staining (green) and increased activated caspase-3 expression (red). Images in (a)–(d) are representative of three separate experiments. (e) Co-incubation of cells [primary cortical neurons (left) or HT22 cells (right)] with 20 μM zVAD-FMK, a broad-spectrum caspase inhibitor, caused a significant reduction in cell death following 24 h treatment with 15-A2t-IsoP as assessed by lactate dehydrogenase (LDH) release (neurons) or MTT assay (HT22s). Data represent the mean + SEM of four independent experiments, each performed in triplicate and analyzed by two-tailed paired t-test. !p < 0.05 vs. control, *p < 0.05 vs. IsoP + zVAD.