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. 2017 Dec 4;15(12):378. doi: 10.3390/md15120378

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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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A 24 h incubation with Lobocrassin B at concentrations of 2.5 and 5 μM caused mitochondrial dysfunction and ROS accumulation in CL1-5 and H520 cells. (A) The dissipation of ΔΨm was observed detecting by stained with JC-1 dye and analyzed by flow cytometry. (B) Lobocrassin B enhanced the levels of Bax and reduced the expression of Bcl-2. The fold of band intensity compared to related controls was marked respectively. (C) Lobocrassin B also increased intracellular reactive oxygen species (ROS) levels by stained with DCFH-DA dye and analyzed by flow cytometry. The bar data shown represent the mean ± SD of samples from three wells. * p < 0.05; ** p < 0.01; *** p < 0.001 compared to control group (One-Way ANOVA). All data are representative of at least three independent experiments.

A 24 h incubation with Lobocrassin B at concentrations of 2.5 and 5 μM caused mitochondrial dysfunction and ROS accumulation in CL1-5 and H520 cells. (A) The dissipation of ΔΨm was observed detecting by stained with JC-1 dye and analyzed by flow cytometry. (B) Lobocrassin B enhanced the levels of Bax and reduced the expression of Bcl-2. The fold of band intensity compared to related controls was marked respectively. (C) Lobocrassin B also increased intracellular reactive oxygen species (ROS) levels by stained with DCFH-DA dye and analyzed by flow cytometry. The bar data shown represent the mean ± SD of samples from three wells. * p < 0.05; ** p < 0.01; *** p < 0.001 compared to control group (One-Way ANOVA). All data are representative of at least three independent experiments.