Melatonin alleviates myosin light chain kinase expression and activity via the mitogen‑activated protein kinase pathway during atherosclerosis in rabbits

Cheng,Xiaowen; Wan,Yufeng; Xu,Yuanhong; Zhou,Qing; Wang,Yuan; Zhu,Huaqing

doi:10.3892/mmr.2014.2753

Melatonin alleviates myosin light chain kinase expression and activity via the mitogen‑activated protein kinase pathway during atherosclerosis in rabbits

Authors:
- Xiaowen Cheng
- Yufeng Wan
- Yuanhong Xu
- Qing Zhou
- Yuan Wang
- Huaqing Zhu
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Affiliations: Laboratory of Molecular Biology and Department of Biochemistry, Anhui Medical University, Hefei, Anhui 230032, P.R. China, Department of Otolaryngology, The Affiliated Chaohu Hospital of Anhui Medical University, Hefei, Anhui 230032, P.R. China, Department of Clinical Laboratory, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230032, P.R. China
Published online on: October 23, 2014 https://doi.org/10.3892/mmr.2014.2753
Pages: 99-104
Copyright: © Cheng et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 3.0].

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Abstract

Melatonin (MLT) is an endogenous indole compound with numerous biological activities that has been associated with atherosclerosis (AS). In the present study, rabbits were used as an AS model in order to investigate whether MLT affects endothelial cell permeability, myosin light chain kinase (MLCK) activity and MLCK expression via the mitogen‑activated protein kinase (MAPK) pathway. Expression and activity of MLCK were measured using western blot analysis, quantitative polymerase chain reaction, immunohistochemistry and γ‑32P‑adenosine triphosphate incorporation. Endothelial permeability was detected using rhodamine phalloidin fluorescence staining. The phosphorylation of extracellular regulated protein kinase (ERK), c‑Jun N‑terminal kinase (JNK) and p38 in endothelial cells were also analyzed using western blot analysis. Atheromatous plaques were formed in rabbits with a high cholesterol diet; however, following treatment with MLT, the number and areas of atheromatous plaques were significantly reduced. In addition, MLT treatment reversed the increase of MLCK activity and expression that occurred in rabbits with high cholesterol intake. Furthermore, levels of phosphorylated ERK, JNK and p38 decreased following MLT treatment. In conclusion, the results of the present study indicated that AS may be associated with increased MLCK expression and activity, which was reduced following treatment with MLT. The mechanism of action of MLT was thought to proceed via modulating MAPK pathway signal transduction; however, further studies are required in order to fully elucidate the exact regulatory mechanisms involved.

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