Evidence-based antioxidant activity of the essential oil from Fructus A. zerumbet on cultured human umbilical vein endothelial cells’ injury induced by ox-LDL
1 Research Division of Pharmacology, Guiyang Medical University, Guiyang 55004, People’s Republic of China
2 Department of Pharmaceutics, Guiyang Medical University, Guiyang 55004, People’s Republic of China
BMC Complementary and Alternative Medicine 2012, 12:174 doi:10.1186/1472-6882-12-174Published: 7 October 2012
The essential oil from Fructus Alpiniae zerumbet (FAZ) is its principal bioactive ingredient, and is widely used in Miao folk herbs in Guizhou province for the treatment of gastrointestinal and cardiovascular diseases. Several studies have confirmed that FAZ ameliorates hyperlipidemia and atherosclerosis. Because endothelial dysfunction often accompanies cardiovascular diseases, especially hyperlipidemia and atherosclerosis, the present study concentrated on evaluating the endothelial protective effects of the essential oil from FAZ (EOFAZ) on oxidized low-density lipoprotein (ox-LDL)-induced injury of cultured human umbilical vein endothelial cells (HUVECs) and on the regulation of oxidative stress.
Cell viability was analyzed with the MTT assay and trypan blue exclusion staining (TBES). Cell injury was assessed by lactate dehydrogenase (LDH) release. Biochemical enzymatic methods were used to evaluate the oxidative stress, including the lipid peroxidation product, malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px).
The redox status of HUVECs was significantly exacerbated after exposure to ox-LDL. EOFAZ protected HUVECs against ox-LDL injury as assessed by the MTT assay, TBES and LDH release. Furthermore, EOFAZ ameliorated the oxidative stress by elevating the activities of SOD, CAT and GSH-Px, and increasing the GSH levels, in addition to attenuating the MDA contents.
The present data provide the first experimental evidence that EOFAZ protects endothelial cells against ox-LDL-induced injury, and indicate that this protection involves ameliorating the redox status.