Fig. 2.

Hypoxic preconditioning attenuates cytotoxicity induced by potassium deprivation, glutamate, or 3-NP. A, CGN were exposed to 5% O₂ for 9 hr (black bars) or not (white bars), reoxygenated for subsequent 24 hr, and challenged with potassium deprivation, 100 μm glutamate (Glut), or 500 μm 3-NP for 24 hr. Viability was assessed by FDA staining. B, CGN were treated as in A, and caspase-3 activity was measured by the cleavage of DEVD-amc (12.5 μm) at 6 hr after potassium deprivation or exposure to glutamate. Data are expressed as means ± SEM from three independent experiments performed in triplicate (*p< 0.05; **p < 0.01 compared with normoxic controls). C, CGN were treated according to the schedule displayed in A (black bars andwhite bars) or with CHX (10 μg/ml) in addition to incubation for 9 hr at 5% O₂ and for another 15 hr before switching to regular parallel conditioned medium (dotted bars). Data are expressed as means ± SEM from three independent experiments performed in triplicate (*p< 0.05; **p < 0.01; ANOVA, followed by Tukey'spost hoc test compared with hypoxic but not with CHX-treated controls). HK, High K⁺;LK, low K⁺.