The Endothelial Protective Properties of Essential Oil from Fructus Alpiniae zerumbet via the Akt/NOS-NO Signaling Pathway In Vitro.

Autor: Tingting Xiao, Yu Zeng, Yini Xu, Yanyan Zhang, Yan Jiang, Ling Tao, Xiangchun Shen
Předmět:
Zdroj: Planta Medica; 2014, Vol. 80 Issue 17, p1628-1634, 7p
Abstrakt: Oxidized low-density lipoprotein has been demonstrated to induce vascular injury, at least partly, through the nitric oxide-dependent pathway. Our previous studies showed that the essential oil from Fructus Alpiniae zerumbet had a capacity of antioxidation to ameliorate endothelial function and vasodilatation on aortic rings ex vivo. The present study aims to confirm the hypothesis that Fructus Alpiniae zerumbet protects against oxidized low-density lipoprotein-induced endothelial dysfunction in human aortic endothelial cells, and the role nitric oxide synthase plays in the process. Human aortic endothelial cells were pretreated with one of three different doses of Fructus Alpiniae zerumbet (1, 2, or 4pg/mL), simvastatin (10 pM), or vehicle, followed by coincubation with oxidized low-density lipoprotein (150pg/mL), for designed time periods. Exposure to oxidized low-density lipoprotein resulted in cytotoxicity accompanied by mitochondrial membrane potential collapse, excessive reactive oxygen species generation, and a decrease of nitric oxide production. The upregulation of inducible nitric oxide synthase mRNA and protein expression was determined by reverse transcription- polymerase chain reaction and Western blot analysis, respectively. Furthermore, oxidized lowdensity lipoprotein inhibited Akt phosphorylation and downregulated endothelial nitric oxide synthase and soluble guanylatecyclase in mRNA expression and the protein level. However, cytotoxicity and aberrant reactive oxygen species and nitric oxide generation caused by oxidized lowdensity lipoprotein could be significantly inhibited by Fructus Alpiniae zerumbet or Sim pretreatment. Results from this study confirmed that Fructus Alpiniae zerumbet could protect against oxidized low-density lipoprotein-induced endothelial dysfunction by antioxidation and modulating the Akt/nitric oxide synthase-nitric oxide signaling pathway. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index