Protective effects of sasanquasaponin on injury of endothelial cells induced by anoxia and reoxygenation in vitro.
The protective effects of sasanquasaponin, an effective compound from Chinese traditional herbs, on ischaemia and reperfusion injury in mouse hearts have been suggested through modulation of intracellular Cl(-) homeostasis. The effects of sasanquasaponin on injury of endothelial cells, however, induced by anoxia and reoxygenation remain unknown. Therefore, the present study attempted to observe the effects of sasanquasaponin on anoxia and reoxygenation injury in endothelial cells and investigate its putative mechanisms. Human umbilical vein endothelial cells (HUVECs) were exposed to normoxia or anoxia and reoxygenation in the absence or presence of sasanquasaponin (10.0, 1.0 and 0.1 micromol/l). Lactate dehydrogenase activity was determined in cultured HUVECs supernatant, and malondialdehyde content, superoxide dismutase and glutathione peroxidase activities were measured in HUVECs by a colorimetric method. Neutrophil adhesion to HUVECs was assayed colorimetrically. The levels of intercellular adhesion molecule-1 and tumour necrosis factor-alpha were detected. The activity of nuclear factor kappa B was determined by flow cytometry. The results show that sasanquasaponin decreased the lactate dehydrogenase activity and malondialdehyde contents, and inhibited the neutrophil adhesion to HUVECs; sasanquasaponin, moreover, inhibited nuclear factor kappa B transnuclear activity, lowered tumour necrosis factor-alpha and intercellular adhesion molecule-1 expression levels. On the other hand, sasanquasaponin increased the mitochondrial superoxide dismutase and glutathione peroxidase activities. It is suggested that sasanquasaponin could protect HUVECs against anoxia and reoxygenation injury, and the protective mechanisms appear to be related to anti-lipoperoxidation and anti-adhesion.
Huang
Qiren
Q
Jiangxi Provincial Key Laboratory of Molecular Medicine at the Second Affiliated Hospital, Nanchang University, Nanchang, China.
He
Ming
M
Chen
Heping
H
Shao
Lijian
L
Liu
Dan
D
Luo
Yongming
Y
Dai
Yucheng
Y
D002448:Cell Adhesion / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D042783:Endothelial Cells / Q000187:drug effects*; D005979:Glutathione Peroxidase / Q000378:metabolism; D006801:Humans; D000860:Hypoxia / Q000473:pathology*; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008315:Malondialdehyde / Q000378:metabolism; D024101:Mitochondrial Proteins / Q000378:metabolism; D016328:NF-kappa B / Q000378:metabolism; D009504:Neutrophils / Q000187:drug effects / Q000378:metabolism; D010100:Oxygen / Q000633:toxicity*; D020011:Protective Agents; D012503:Saponins / Q000627:therapeutic use*; D013482:Superoxide Dismutase / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
C497504:22-O-angeloylcamelliagenin C-3-O-(glucopyranosyl-1-2)(glucopyranosyl-1-2-O-arabinopyranosyl-1-3-)glucopyranosiduronic acid; D024101:Mitochondrial Proteins; D016328:NF-kappa B; D020011:Protective Agents; D012503:Saponins; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D008315:Malondialdehyde; D007770:L-Lactate Dehydrogenase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D010100:Oxygen