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Ligustrazine improves atherosclerosis in rat via attenuation of oxidative stress
Liu Chang 1 *,Jiang Fengrong 2,Chen Siyu 3,Zhang Wenbo 3,Qian Jinchun 3
1.Jiangsu Key Laboratory for Molecular and Medical Biotechnology, Nanjing Normal University
2.College of Pharmacy, Nanjing University of Traditional Chinese Medicine, Nanjing, China,210029
3.Jiangsu Key Laboratory for Molecular and Medical Biotechnology, Nanjing Normal University, Nanjing, China, 210046
*Correspondence author
#Submitted by
Subject:
Funding: grants from the Chinese National Science Foundation (No.30870928),Research Fund for the Doctoral Program of Higher Education of China)
Opened online: 3 January 2011
Accepted by: none
Citation: Liu Chang,Jiang Fengrong,Chen Siyu.Ligustrazine improves atherosclerosis in rat via attenuation of oxidative stress[OL]. [ 3 January 2011] http://en.paper.edu.cn/en_releasepaper/content/4401385
 
 
Context: Ligustrazine (Lig) is a compound isolated from the rhizome of Ligusticum walliichi (Ligusticum Chuanxiong Hort) and has been reported to be effective for the treatment of a variety of vascular diseases.Objective: The anti-atherosclerotic activities of Lig are evaluated in vivo for the first time in the present study. Materials and methods: We gave rats a single injection of vitamin D3 and then fed them with an atherogenic diet for 6 weeks to induce atherosclerosis. Lig was simultaneously given to rats by gavage in the therapy groups. The effects of Lig on blood parameters, aorta and liver histology, and gene expression were investigated. In addition, the solely effects of Lig on food intake, body weight gain, and taste preference were also evaluated.Results: We found that Lig decreased the total cholesterol, triglyceride, and low density lipoprotein levels while it increased high density lipoprotein level in the plasma. The circulating endothelial cells were also decreased in Lig-treated rats, indicating the attenuation of endothelial injury. In contrast, Lig restored the total antioxidant capacity and SOD1 activity while decreasing the MDA generation. Furthermore, Lig improved liver dysfunction by decreasing ALT and AST levels. Histological examinations revealed that Lig suppressed atherosclerotic plaque progression in the thoracic aorta and lipid accumulation in the liver. At the transcriptional level, Lig inhibited the induction of antioxidant genes both in aorta and in liver. Lig also suppressed the mRNA expression of the genes involved in the hepatic fatty acid oxidation. Finally, Lig had a minimum effect on food intake, body weight gain, and taste preference.Discussion and conclusion: Our results suggest that Lig suppresses the development of atherosclerosis and hepatic lipid accumulation via the alleviation of oxidative stress and the improvement of dyslipidemia.
Keywords:Ligustrazine;atherosclerosis;oxidative stress;dyslipidemia
 
 
 

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