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J Cell Physiol. 2019 Feb;234(2):1758-1767. doi: 10.1002/jcp.27046. Epub 2018 Aug 26.

Rosmarinic acid inhibits nicotine-induced C-reactive protein generation by inhibiting NLRP3 inflammasome activation in smooth muscle cells.

Yao Y1,2,3, Mao J4, Xu S5, Zhao L6, Long L4, Chen L4, Li D1,2, Lu S1,2.

Author information

1
Department of Biochemistry and Molecular Biology, School of Basic Medical Science, Xi'an Jiaotong University Health Science Center, Xi'an, China.
2
Key Laboratory of Environment and Genes Related to Diseases, Xi'an Jiaotong University, Ministry of Education of China, Xi'an, China.
3
Department of Central Laboratory, The First Affiliated Hospital of Xi'an Medical University, Xi'an, China.
4
Department of Pharmacology, The First Affiliated Hospital of Xi'an Medical University, Xi'an, China.
5
Department of Pharmacology, Xi'an Jiaotong University School of Medicine, Xi'an, China.
6
Department of Molecular Physiology and Biophysics, Holden Comprehensive Cancer Center, University of Iowa, Carver College of Medicine, Iowa City, Iowa.

Abstract

Atherosclerosis is widely known to be a chronic inflammatory disease. C-reactive protein (CRP), an important inflammatory factor, plays an essential role in the pathogenesis of atherosclerosis. Nicotine, the main addictive component of cigarette, has been shown to induce the production of CRP. The aim of this study was to investigate the effect of rosmarinic acid (RA), a polyphenol with antiinflammatory activity, on nicotine-induced elevation of CRP in vascular smooth muscle cells (VSMCs). We found that pretreatment of VSMCs with RA attenuated nicotine-induced expression of CRP in a time- and dose-dependant manner. In addition, RA also inhibited the activation of NLR family pyrin domain containing 3 (NLRP3) inflammasome and reactive oxygen species (ROS) production resulting from nicotine treatment in VSMCs. To confirm these findings in vivo, we constructed a nicotine-induced atherosclerosis rat model. RA did not significantly reduce the serum nicotine level of the rats, whereas it significantly decreased the levels of serum lipids, including concentrations of cholesterol, triglycerides, and low-density lipoprotein cholesterol, and the serum level of CRP. RA also led to diminished nicotine-induced activation of NLRP3 inflammasome and elevation in the CRP level in the aortic tissue of the model rats. The results of this study suggested a protective role of RA in nicotine-induced atherosclerosis by inhibiting the ROS-NLRP3 inflammasome-CRP axial, and RA therefore represented a potential effective therapeutic approach to atherosclerosis, in particular for those who smoke.

KEYWORDS:

CRP; NLRP3 inflammasome; atherosclerosis; nicotine; rosmarinic acid

PMID:
30146678
DOI:
10.1002/jcp.27046

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