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. 2017 Jan 13;22(1):124. doi: 10.3390/molecules22010124

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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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JNK/p38 pathways played protect role in olaquindox-induced DNA damage. (A) HepG2 cells were treated with olaquindox (400 µg/mL) for 4 h after preincubation with SP600125 or SB203580 for 1 h; (B) % tail DNA; (C) tail length; (D) tail moment; (E) HepG2 cells were treated with olaquindox (400 µg/mL) for 24 h after preincubation with SP600125 or SB203580 for 1 h. Cells were observed under a Leica inverted fluorescence microscope (400×). 1000 binucleated cells were recorded from each experiment and three independent experiments were carried out. All results were presented as mean ± SD. (** p < 0.01, compared with the control group; # p < 0.05, compared to olaquindox group).

JNK/p38 pathways played protect role in olaquindox-induced DNA damage. (A) HepG2 cells were treated with olaquindox (400 µg/mL) for 4 h after preincubation with SP600125 or SB203580 for 1 h; (B) % tail DNA; (C) tail length; (D) tail moment; (E) HepG2 cells were treated with olaquindox (400 µg/mL) for 24 h after preincubation with SP600125 or SB203580 for 1 h. Cells were observed under a Leica inverted fluorescence microscope (400×). 1000 binucleated cells were recorded from each experiment and three independent experiments were carried out. All results were presented as mean ± SD. (** p < 0.01, compared with the control group; # p < 0.05, compared to olaquindox group).