Lingyan Wu1, Guixue Wang, Shutang Tang, Guang Long, Tieying Yin. 1. Key Laboratory of Biorheological Science and Technology (Chongqing University), Ministry of Education, Chongqing Engineering Lab. in Vascular Implants, Bioengineering College of Chongqing University, Chongqing, 400044, China.
Abstract
AIMS: It is generally accepted that the oxidative stress and the proliferative activity of vascular smooth muscle cells (VSMCs) contribute to the pathogenesis of neointimal hyperplasia after vascular injury. Although β-elemene (β-1-methyl-1-vinyl-2, 4-diisopropenyl-cyclohexane) has been used as an antitumour drug, its therapeutic effect on vascular diseases has not yet been determined. In this study, we investigated whether β-elemene could inhibit oxidative damage of vascular endothelial cells, suppress VSMCs growth and prevent neointimal hyperplasia. METHODS AND RESULTS: β-elemene can increase the survival rate of human umbilical vein endothelial cells in vitro. By measuring the malondialdehyde content, total antioxidant capacity, superoxide dismutase activity, catalase activity, glutathione peroxidase activity and nitric oxide levels, we assessed the protective effect of β-elemene in the vascular endothelium model against oxidant-induced injury. Μoreover, β-elemene inhibited cell proliferation and induced apoptosis in cultured VSMCs. In a flow culture system, β-elemene reduced the migration distance of VSMCs. By transwell migration assay, β-elemene was found to reduce the migration cell number of VSMCs, but not affect the HUVECs migration. In a rat carotid artery balloon injury model, administration of β-elemene significantly reduced the ratio of intimal area to medial area and neointima formation. CONCLUSIONS: Our results indicate that β-elemene is effective in protecting the endothelial cells from injury induced by hydrogen peroxide in vitro, inhibiting smooth muscle cell proliferation/migration and inhibiting neointima formation in vivo after vascular injury.
AIMS: It is generally accepted that the oxidative stress and the proliferative activity of vascular smooth muscle cells (VSMCs) contribute to the pathogenesis of neointimal hyperplasia after vascular injury. Although β-elemene (β-1-methyl-1-vinyl-2, 4-diisopropenyl-cyclohexane) has been used as an antitumour drug, its therapeutic effect on vascular diseases has not yet been determined. In this study, we investigated whether β-elemene could inhibit oxidative damage of vascular endothelial cells, suppress VSMCs growth and prevent neointimal hyperplasia. METHODS AND RESULTS: β-elemene can increase the survival rate of human umbilical vein endothelial cells in vitro. By measuring the malondialdehyde content, total antioxidant capacity, superoxide dismutase activity, catalase activity, glutathione peroxidase activity and nitric oxide levels, we assessed the protective effect of β-elemene in the vascular endothelium model against oxidant-induced injury. Μoreover, β-elemene inhibited cell proliferation and induced apoptosis in cultured VSMCs. In a flow culture system, β-elemene reduced the migration distance of VSMCs. By transwell migration assay, β-elemene was found to reduce the migration cell number of VSMCs, but not affect the HUVECs migration. In a rat carotid artery balloon injury model, administration of β-elemene significantly reduced the ratio of intimal area to medial area and neointima formation. CONCLUSIONS: Our results indicate that β-elemene is effective in protecting the endothelial cells from injury induced by hydrogen peroxide in vitro, inhibiting smooth muscle cell proliferation/migration and inhibiting neointima formation in vivo after vascular injury.