Journal
ULTRASOUND IN MEDICINE AND BIOLOGY
Volume 44, Issue 4, Pages 853-860Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.ultrasmedbio.2017.12.016
Keywords
Emodin; Sonodynamic therapy; Macrophages; Oxidation
Funding
- National Natural Science Foundation of China [81301343]
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In previous studies, sonodynamic therapy mediated by emodin (emodin-SDT) induced cytoskeletal filament disruption and apoptosis of THP-1-derived macrophages. In this research, we investigated the underlying mechanism. THP-1-derived macrophages were incubated with emodin and exposed to ultrasound irradiation. After emodin-SDT, we measured the production of reactive oxygen species (ROS) and analyzed the level of amino acid oxidation in microtubules, the cleavage of microtubules and the mitochondrial membrane potential (MMP). We found that intracellular emodin accumulated mainly on microtubules. After emodin-SDT, generation of ROS was evident. Analysis of the carbonyl content of proteins suggested oxidation of microtubules. Microtubules were disrupted after emodin-SDT, and the antioxidant N-acetyl-L-cysteine prevented this disruption. MMP decreased after emodin-SDT, and this effect could be prevented by N-acetyl-L-cysteine. We conclude that emodin-SDT induces the generation of ROS. The oxidation of microtubules leads to its cleavage and the subsequent decline in MMP. (C) 2018 World Federation for Ultrasound in Medicine & Biology. All rights reserved.
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