Propofol protects against anandamide-induced injury in human umbilical vein endothelial cells.
Endocannabinoid anandamide, arachidonylethanolamine (AEA), is considered to be a causative mediator of hemorrhagic or septic shock, inducing death of several types of cells by producing free radicals such as reactive oxygen species (ROS). Propofol contains a phenolic hydroxyl group that donates electrons to the free radicals, and thus functions as an antioxidant. The purpose of this study was to investigate the protective effect of propofol against AEA-induced cell injury. After incubation with propofol at concentrations of 10, 50 or 100 µM, human umbilical vein endothelial cells (HUVECs) were stimulated with 10 µM of AEA for 24 h. ROS production, caspase-3 activity, and cell viability were evaluated 1, 8, and 24 h after the administration of 10 µM of AEA, respectively. Propofol (50 µM) significantly attenuated cell death induced by AEA, showing a protective effect against ROS production and caspase-3 activity. These results suggest that propofol at concentrations used during clinical anesthesia protects HUVECs against AEA-induced injury, in part by suppressing apoptosis.
Department of Anesthesiology, Kurume University School of Medicine, Kurume, Japan.
Takahiko
T
Ito
Yasunori
Y
Mishima
Asuka
A
Ito
Naomitsu
N
Kameyama
Hideki
H
Harada
Osuke
O
Iwata
Seiji
S
Watanabe
Kazuo
K
Ushijima
D000581:Amidohydrolases / Q000378:metabolism; D018686:Anesthetics, Intravenous / Q000627:therapeutic use; D000975:Antioxidants / Q000378:metabolism; D017209:Apoptosis; D001095:Arachidonic Acids / Q000009:adverse effects*; D002121:Calcium Channel Blockers / Q000009:adverse effects; D053148:Caspase 3 / Q000378:metabolism; D002470:Cell Survival; D004305:Dose-Response Relationship, Drug; D063388:Endocannabinoids; D061307:Human Umbilical Vein Endothelial Cells / Q000166:cytology / Q000187:drug effects*; D006801:Humans; D017665:Hydroxyl Radical; D053284:Polyunsaturated Alkamides / Q000009:adverse effects*; D015742:Propofol / Q000627:therapeutic use*; D017382:Reactive Oxygen Species; D013997:Time Factors; D016896:Treatment Outcome; D057772:Vascular System Injuries / Q000139:chemically induced*; D000099252:Fatty Acid Amide Hydrolases
D000581:Amidohydrolases; D018686:Anesthetics, Intravenous; D000975:Antioxidants; D001095:Arachidonic Acids; D002121:Calcium Channel Blockers; D053148:Caspase 3; D063388:Endocannabinoids; D017665:Hydroxyl Radical; D053284:Polyunsaturated Alkamides; D015742:Propofol; D017382:Reactive Oxygen Species; D000099252:Fatty Acid Amide Hydrolases; C078814:anandamide