TY - JOUR
T1 - Intravenous low redox potential saline attenuates FeCl 3-induced vascular dysfunction via downregulation of endothelial H 2O 2, CX3CL1, intercellular adhesion molecule-1, and p53 expression
AU - Chen, Da Lung
AU - Chen, Tzen Wen
AU - Chien, Chiang Ting
AU - Li, Ping Chia
PY - 2011/5
Y1 - 2011/5
N2 - Exaggerated reactive oxygen species (ROS) may contribute to vascular injury by the enhancement of CX3CL1, intercellular adhesion molecule-1 (ICAM-1), and pro-apoptotic p53 expression. Reduced water with safely antioxidant activity may protect vascular tissue against oxidative injury. We established reduced water (RW) by using a modified magnesium alloy and evaluated the effects of an RW-made culture medium on TNF-α-induced endothelial damage in vitro and intravenous RW-made saline (0.9%NaCl) infusion on FeCl 3-induced arterial injury in rats in vivo. Several oxidative stresses were evaluated by using a chemiluminescence analyzer, Western blot, and immunohistochemistry. We found that the established RW, RW-culture medium, and RW saline displayed a lower redox potential (2O 2 scavenging activity compared with distilled-water-made solutions. The RW-culture medium significantly depressed TNF-α-enhanced endothelial H 2O 2 production; improved CX3CL1, ICAM-1, and p53 expression; and inhibited activated monocyte adhesion to endothelial cells as well as to the CX3CL1 or the ICAM-1 coated plate when compared with the distilled-water-culture medium. In the in vivo study, the time required for FeCl 3-induced occlusion in the urethane anesthetized rat's carotid and femoral arteries was significantly extended by intravenous RW saline infusion compared with distilled-water saline. FeCl 3 stimulation significantly enhanced vascular NADPH oxidase activity, ROS production, as well as CX3CL1, ICAM-1, p53, 3-nitrotyrosine, and 4-hydroxynonenal expression in the damaged arteries. Intravenous RW saline significantly reduced all the FeCl 3-enhanced oxidative parameters when compared with intravenous distilled-water-saline infusion. We conclude that the RW-culture medium and saline made from magnesium alloy confer cardiovascular protection by the antioxidant capability.
AB - Exaggerated reactive oxygen species (ROS) may contribute to vascular injury by the enhancement of CX3CL1, intercellular adhesion molecule-1 (ICAM-1), and pro-apoptotic p53 expression. Reduced water with safely antioxidant activity may protect vascular tissue against oxidative injury. We established reduced water (RW) by using a modified magnesium alloy and evaluated the effects of an RW-made culture medium on TNF-α-induced endothelial damage in vitro and intravenous RW-made saline (0.9%NaCl) infusion on FeCl 3-induced arterial injury in rats in vivo. Several oxidative stresses were evaluated by using a chemiluminescence analyzer, Western blot, and immunohistochemistry. We found that the established RW, RW-culture medium, and RW saline displayed a lower redox potential (2O 2 scavenging activity compared with distilled-water-made solutions. The RW-culture medium significantly depressed TNF-α-enhanced endothelial H 2O 2 production; improved CX3CL1, ICAM-1, and p53 expression; and inhibited activated monocyte adhesion to endothelial cells as well as to the CX3CL1 or the ICAM-1 coated plate when compared with the distilled-water-culture medium. In the in vivo study, the time required for FeCl 3-induced occlusion in the urethane anesthetized rat's carotid and femoral arteries was significantly extended by intravenous RW saline infusion compared with distilled-water saline. FeCl 3 stimulation significantly enhanced vascular NADPH oxidase activity, ROS production, as well as CX3CL1, ICAM-1, p53, 3-nitrotyrosine, and 4-hydroxynonenal expression in the damaged arteries. Intravenous RW saline significantly reduced all the FeCl 3-enhanced oxidative parameters when compared with intravenous distilled-water-saline infusion. We conclude that the RW-culture medium and saline made from magnesium alloy confer cardiovascular protection by the antioxidant capability.
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U2 - 10.1016/j.trsl.2010.12.012
DO - 10.1016/j.trsl.2010.12.012
M3 - Article
C2 - 21497778
AN - SCOPUS:79954473718
SN - 1931-5244
VL - 157
SP - 306
EP - 319
JO - Translational Research
JF - Translational Research
IS - 5
ER -
