Abstract
In this paper, the protective effects of the active fraction (SF-7) from Shaofu Zhuyu decoction (SFZYD) were tested on a hydrogen peroxide (H2O2)-induced rat vascular smooth muscle cells (VSMCs) oxidative injury model. This active fraction (SF-7) shows potent antioxidant properties. The cell viability and oxidative damage markers of VSMCs were determined after exposure to H2O2 for 16 hours. It was observed that SF-7 significantly increased cell survival and reduced apoptosis of H2O2-injured VSMCs. Moreover, SF-7 could markedly increase intracellular superoxide dismutase (SOD) activity and decrease the malondialdehyde (MDA) level in H2O2-injured VSMCs, and suppress the generation of intracellular reactive oxygen species (ROS), as well as intracellular Ca2+ concentration. Thus, SF-7 exhibits protective effects against H2O2-injury on VSMCs, which may be associated with its antioxidant properties. It is suggested that SF may be useful in the treatment of blood stasis syndrome in which oxidative injury is mainly implicated.
Highlights
Shaofu Zhuyu decoction (SFZYD), created by Qingren Wang in the Qing Dynasty of China is a Traditional Chinese Medicine formula for treating blood stasis syndrome
SF-7 exhibits protective effects against H2O2-injury on vascular smooth muscle cells (VSMCs), which may be associated with its antioxidant properties
It is suggested that SF may be useful in the treatment of blood stasis syndrome in which oxidative injury is mainly implicated
Summary
Shaofu Zhuyu decoction (SFZYD), created by Qingren Wang in the Qing Dynasty of China is a Traditional Chinese Medicine formula for treating blood stasis syndrome. A recent study showed that SFZYD could significantly inhibit the constriction of uterine smooth muscle and possess anti-inflammatory activity [2]. Excessive ROS are able to produce cellular membrane lipid peroxidation, lipid–protein interaction alteration, enzyme inactivation and DNA breakage, and in the end, to cause cell injury (e.g. vascular endothelial cells and vascular smooth cells), apoptosis or necrosis. These detrimental effects are attributed to enhancing intracellular ROS and Ca2+. The aim of this study may provide scientific information to further understanding of the mechanism of action of this formula in blood stasis syndrome
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