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. Author manuscript; available in PMC: 2013 Feb 1.

Published in final edited form as: Neurosurgery. 2012 Feb;70(2):497–510. doi: 10.1227/NEU.0b013e31823209cf

Induction of cell death by JS-K involves regulation by several signalling pathways leading to apoptosis. A. The cytotoxic effect of JS-K in U87 cells can be modified by pre-treatment with Z-VAD-FMK (50 μM), QVD-OPH (20μM), U0126 (10 μM), ODQ (100 μM) or sulfasalazine (50 μM) for 2 hours prior to the 24 h incubation period with JS-K (15μM). Cell viability was assessed by MTT test. B. JS-K induces apoptosis in U87 cells associated with caspase-3 activation. Cells were treated with JS-K (15 μM) for 24 hours, and caspase-3 activity was assessed at the end of the incubation. Data from MTT and caspase-3 assays are expressed as means ± SEM from three independent experiments. # indicates a significant difference compared to the control (p< .05), * and ** refer to statistical testing against JS-K monotherapy with p-values of p< .05 and p< .0001, respectively.

Induction of cell death by JS-K involves regulation by several signalling pathways leading to apoptosis. A. The cytotoxic effect of JS-K in U87 cells can be modified by pre-treatment with Z-VAD-FMK (50 μM), QVD-OPH (20μM), U0126 (10 μM), ODQ (100 μM) or sulfasalazine (50 μM) for 2 hours prior to the 24 h incubation period with JS-K (15μM). Cell viability was assessed by MTT test. B. JS-K induces apoptosis in U87 cells associated with caspase-3 activation. Cells were treated with JS-K (15 μM) for 24 hours, and caspase-3 activity was assessed at the end of the incubation. Data from MTT and caspase-3 assays are expressed as means ± SEM from three independent experiments. # indicates a significant difference compared to the control (p< .05), * and ** refer to statistical testing against JS-K monotherapy with p-values of p< .05 and p< .0001, respectively.