title: Allicin prevents oxidized low-density lipoprotein-induced endothelial cell injury by inhibiting apoptosis and oxidative stress pathway.
abstract: BACKGROUND
  Vascular endothelial apoptosis is significantly associated with atherosclerosis and cardiovascular diseases, for which oxidized low-density lipoprotein (ox-LDL) is a major risk factor. Allicin, the primary active ingredient of garlic, has been found to have cardiovascular protective effect by changing the fatty-acid composition, but its effect on ox-LDL-induced vascular endothelial injury remains unclear. We investigated the protective effect of allicin on cell viability, LDH release, apoptosis and apoptotic signaling in human umbilical vein endothelial cells (HUVECs).
  
  
  METHODS
  In cultured HUVEC cell line, ox-LDL induced injury was investigated. The cell viability and injury were evaluated by using cell proliferation Assay kit and LDH release assay. The apoptosis was evaluated by the Annexin V-FITC kit. The activity of caspase-3 was assessed using a colorimetric caspase-3 assay kit. The ROS production was evaluated by fluorometric assay and NADPH oxidase activity was assessed with a GENMED kit.
  
  
  RESULTS
  Exposure of HUVECs to ox-LDL (150 μg/ml) reduced cell viability, induced apoptosis and increased activity of caspase-3, NADPH oxidase, and reactive oxygen species (ROS) production. The pretreatment with allicin (30 and 100 μM) significantly rescued the cell viability, inhibited ox-LDL-induced apoptosis and activity of caspase-3, NADPH oxidase and ROS production in HUVECs, and the protective effect is concentration-dependent. The allicin (100 μM) alone did not show significant difference from control. Our study demonstrated that allicin protected HUVECs from ox-LDL-induced endothelial injury by reducing the apoptosis, mediated by inhibition of caspase-3 and NADPH oxidase related apoptotic signaling.
  
  
  CONCLUSIONS
  Allicin prevents ox-LDL-induced endothelial cell injury by inhibiting apoptosis and oxidative stress pathway.
authors.affiliation: Department of Cardiology, Wenzhou People's Hospital, No. 57, Canghou Street, Wenzhou, 325000, China.
authors.forename: Xiaoshu
authors.initials: X
authors.lastname: Chen
authors.affiliation: Department of Cardiology, Wenzhou People's Hospital, No. 57, Canghou Street, Wenzhou, 325000, China.
authors.forename: Sunian
authors.initials: S
authors.lastname: Pang
authors.affiliation: Department of Cardiology, Wenzhou People's Hospital, No. 57, Canghou Street, Wenzhou, 325000, China.
authors.forename: Jianfeng
authors.initials: J
authors.lastname: Lin
authors.affiliation: Department of Cardiology, Wenzhou People's Hospital, No. 57, Canghou Street, Wenzhou, 325000, China.
authors.forename: Jianlan
authors.initials: J
authors.lastname: Xia
authors.affiliation: Department of Cardiology, Wenzhou People's Hospital, No. 57, Canghou Street, Wenzhou, 325000, China. 18057729871@163.com.
authors.forename: Yi
authors.initials: Y
authors.lastname: Wang
mesh_terms: D017209:Apoptosis / Q000187:drug effects*; D002316:Cardiotonic Agents / Q000494:pharmacology*; D053148:Caspase 3 / Q000378:metabolism; D002460:Cell Line; D002470:Cell Survival / Q000187:drug effects; D004220:Disulfides; D004730:Endothelium, Vascular / Q000187:drug effects*; D005737:Garlic / Q000737:chemistry; D006801:Humans; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008077:Lipoproteins, LDL / Q000037:antagonists & inhibitors*; D018384:Oxidative Stress / Q000187:drug effects*; D013441:Sulfinic Acids / Q000494:pharmacology*
chemical_list: D002316:Cardiotonic Agents; D004220:Disulfides; D008077:Lipoproteins, LDL; D013441:Sulfinic Acids; C099252:oxidized low density lipoprotein; C006452:allicin; D007770:L-Lactate Dehydrogenase; D053148:Caspase 3
keywords: Allicin; Apoptosis; Endothelial cell; Oxidative stress; Oxidized low-density lipoprotein