Tropical Journal of Pharmaceutical Research

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Original Research Article

Anti-oxidative Effect of Ligustrazine on Treatment and Prevention of Atherosclerosis

Gui-dong Huang, Jian Mao* and Zhong-wei Ji

State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, Wuxi 214122, PR China

*For correspondence: Email: maojiand417@163.com; Tel: +86-510-8532-9062; Fax: +86-510-8591-2155

Received: 11 July 2013 Revised accepted: 24 October 2013

Tropical Journal of Pharmaceutical Research, December 2013; 12(6): 949-957

http://dx.doi.org/10.4314/tjpr.v12i6.13

Abstract

Purpose: To investigate the protective effects of ligustrazine on oxidative stress-induced atherosclerosis.

Methods: The indicators related to oxidative stress were determined using commercially available assay kits. MTT assay was used to assess the survival rate of human umbilical vein endothelial cells (HUVECs). HUVECs apoptosis was analyzed using fluorescence staining and flow cytometry. mRNA expression level and activity of caspases 3, 8, and 9 were determined via quantitative real-time polymerase chain reaction (PCR) and caspase 3, 8, and 9 assay kits.

Results: Ligustrazine concentration of < 80 µmol/L had negligible inhibitory effect on HUVECs viability and protected HUVECs against oxygen stress damage by regulating the indicators related to oxidative stress. Flow cytometry results show that ligustrazine ameliorated H₂O₂-induced apoptosis, while the proportion of cells that stepped into early apoptosis and late apoptosis or necrosis were 52.7 and 0.6 %, respectively, in the H₂O₂ group, and 38.2 and 1.3 %, respectively, in the ligustrazine group. In addition, ligustrazine attenuated the up-regulation of caspase 3, 8, and 9 mRNA expression levels and activity.

Conclusion: Ligustrazine can protect HUVECs against H₂O₂-induced injuries by regulating the indicators related to oxidative stress and suppressing the overexpression of caspases 3, 8, and 9. The protective mechanism of ligustrazine on H₂O₂-induced injury in HUVECs may be a caspase-dependent anti-apoptotic mechanism which provide important information for treating and preventing oxidative stress-induced atherosclerosis.

Keywords: Ligustrazine, Oxidative stress, Umbilical vein, Endothelial cells, Atherosclerosis