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. 2016 Aug 29;11(8):e0161886. doi: 10.1371/journal.pone.0161886

Fig 6. ROS mediated the mitochondria dysfunction and regulated activation of JNK/p38 in vitamin K2-triggered apoptosis of human bladder cancer T24 cells.

Fig 6

(A). T24 cells were treated with 5mM antioxidant NAC for 1 hour prior to the treatment with or without 100 μM vitamin K2 for 24 hours, then the mitochondria membrane potential was assessed using the Rhodamine 123 dye by flow cytometry. (B). The expression of Bax, Puma and Bcl-2 were changed after treatment with 100 μM vitamin K2 for 24 hours in the present or absent of 5mM antioxidant N-acetyl cysteine (NAC) to human bladder cancer T24 cells. (C). T24 cells were treated 40 μM SP600125(SP) for 1 hour before treatment of 100 μM vitamin K2 for 24 hours, mitochondria membrane potential was evaluated using Rhodamine 123 dye by flow cytometry. (D). T24 cells were treated 10 μM SB203580(SB) for 1 hour before treatment of 100 μM vitamin K2 for 24 hours, mitochondria membrane potential was evaluated using Rhodamine 123 dye by flow cytometry. (E). T24 cells were treated with 5mM NAC for 1 hour before exposure to 100 μM vitamin K2 for 24 hours, then the total proteins were isolated from the cells and activation of JNK/p38 were determined by western blots. ** P<0.01 and *** P<0.001.