Abstract
Objective: To investigate the effect of PPAR γ ligand triglitazone on the secretion of ET-land NO from endothelial cells stimulated by Ang II. Methods: The cultured human umbilical vein endothelial cells (HUVECs) were treated with Ang II and triglitazone. Chemiluminescence analysis was used to measure the concentration of NO, and radioimmunoassay method was used to detect the production of ET-1. Results: The HUVECs were treated with 10 μmol/L and 50 μmol/L triglitazone. The concentration of ET-1 in cell culture supernatants decreased without statistical significance. The concentration of NO increased significantly compared with that of the control (P<0.05). 50 μmol/L triglitazone inhibited the production of Ang II (1 × 10 -6 mol/L) - induced ET-1 obviously (P<0.05), and both 10 μmol/L and 50 μmol/L triglitazone could inhibit the effect of Ang II, which decreased NO release from the endothelial cells, indicating that the concentration of NO increased obviously (P<0.05). Conclusion: Triglitazone can inhibit the effect of Ang II on endothelial cells, which enhances the production of ET-1 but decreases the synthesis and release of NO, showing that triglitazone has relation with the modulation of blood pressure.
| Original language | English |
|---|---|
| Pages (from-to) | 538-540+581 |
| Journal | Journal of Xi'an Jiaotong University (Medical Sciences) |
| Volume | 27 |
| Issue number | 6 |
| State | Published - Dec 2006 |
Keywords
- Angiotensin II
- Hypertension
- Peroxisome proliferator-activated receptor γ (PPARγ)
- Triglitazone
- Vascular active factor
- Vascular endothelial cell
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