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. 2017 Jul 31;18(8):1667. doi: 10.3390/ijms18081667

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© 2017 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Role of mitogen-activated protein kinases (MAPKs) in tricetin-induced apoptotic cell death in HL-60 cells. (A,B) Phosphorylation levels of extracellular signal-regulated kinase (ERK)1/2, p38, and c-Jun N-terminal kinase (JNK)1/2 were assessed by a Western blot analysis after treatment of HL-60 cells with 80 μM tricetin for indicated time points (A) or with various concentrations of tricetin (0~80 μM) for 8 h (B,C) Quantitative results of phopho-ERK1/2, p38, and JNK1/2 protein levels, which were adjusted to the total ERK1/2, p38, and JNK1/2 protein levels and expressed as multiples of induction beyond each respective control. Values are presented as the mean ± SE of three independent experiments. *, ^#, ^&, ^$ p < 0.05, compared to the vehicle control groups; (D,E) HL-60 cells were pretreated with or without 5 μM U0126 or 1 μM JNK-IN-8 for 1 h followed by tricetin (40 μM) treatment for an additional 24 h. Expression levels of cleaved caspases-3, -8, and cell viability were respectively determined by a Western blot analysis (D, left panel) and a CCK-8 assay (E). Quantitative results of cleaved caspase-3 and -8 protein levels, which were adjusted to the β-actin protein level and expressed as multiples of induction beyond each respective control (D, right panel). Values represent the mean ± SE of three independent experiments. * p < 0.05, control vs. tricetin; ^# p < 0.05, tricetin vs. U0126 or JNK-IN-8 plus tricetin.

Role of mitogen-activated protein kinases (MAPKs) in tricetin-induced apoptotic cell death in HL-60 cells. (A,B) Phosphorylation levels of extracellular signal-regulated kinase (ERK)1/2, p38, and c-Jun N-terminal kinase (JNK)1/2 were assessed by a Western blot analysis after treatment of HL-60 cells with 80 μM tricetin for indicated time points (A) or with various concentrations of tricetin (0~80 μM) for 8 h (B,C) Quantitative results of phopho-ERK1/2, p38, and JNK1/2 protein levels, which were adjusted to the total ERK1/2, p38, and JNK1/2 protein levels and expressed as multiples of induction beyond each respective control. Values are presented as the mean ± SE of three independent experiments. *, ^#, ^&, ^$ p < 0.05, compared to the vehicle control groups; (D,E) HL-60 cells were pretreated with or without 5 μM U0126 or 1 μM JNK-IN-8 for 1 h followed by tricetin (40 μM) treatment for an additional 24 h. Expression levels of cleaved caspases-3, -8, and cell viability were respectively determined by a Western blot analysis (D, left panel) and a CCK-8 assay (E). Quantitative results of cleaved caspase-3 and -8 protein levels, which were adjusted to the β-actin protein level and expressed as multiples of induction beyond each respective control (D, right panel). Values represent the mean ± SE of three independent experiments. * p < 0.05, control vs. tricetin; ^# p < 0.05, tricetin vs. U0126 or JNK-IN-8 plus tricetin.