Chlorogenic acid prevents isoproterenol-induced DNA damage in vascular smooth muscle cells

Wang,Jingshuai; Li,Jiyang; Liu,Jie; Xu,Mengjiao; Tong,Xiaowen; Wang,Jianjun

doi:10.3892/mmr.2016.5743

Chlorogenic acid prevents isoproterenol-induced DNA damage in vascular smooth muscle cells

Authors:
- Jingshuai Wang
- Jiyang Li
- Jie Liu
- Mengjiao Xu
- Xiaowen Tong
- Jianjun Wang
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Affiliations: Department of Obstetrics and Gynecology, Shanghai First Maternity and Infant Hospital, Shanghai 201204, P.R. China, Department of General Medicine, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200000, P.R. China, Department of Cardiovascular and Thoracic Surgery, Shanghai East Hospital, Tongji University School of Medicine, Shanghai 200120, P.R. China, Department of Obstetrics and Gynecology, Tongji Hospital of Tongji University, Tongji University School of Medicine, Shanghai 200065, P.R. China
Published online on: September 15, 2016 https://doi.org/10.3892/mmr.2016.5743
Pages: 4063-4068
Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Numerous clinical therapeutic agents have been identified as DNA damaging. The present study revealed that isoproterenol (Iso) resulted in DNA damage in vascular smooth muscle cells (VSMCs) and increased the levels of intracellular oxygen free radicals. Administration of chlorogenic acid (CGA) inhibited this effect. Pretreatment with CGA abrogated the increase in protein expression levels of γ‑H2A histone family member X, phosphorylated ataxia telangiectasia mutated, phosphorylated Rad3‑related protein, breast cancer 1 and C‑terminal Src homologous kinase induced by Iso. In addition, the increase in levels of intracellular reactive oxygen species (ROS) induced by Iso was inhibited by CGA pretreatment in a dose‑dependent manner. The results of the present study suggest that CGA may inhibit Iso‑induced VSMC damage via the suppression of ROS generation. Therefore, CGA may be a novel agent for the treatment of vascular diseases.

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