Total flavonoids from Plumula Nelumbinis suppress angiotensin II-induced fractalkine production by inhibiting the ROS/NF-κB pathway in human umbilical vein endothelial cells
Spandidos Publications -- Experimental and Therapeutic Medicine
DOI 10.3892/etm.2014.1554
Keyword(s)
  1. total flavonoids from Plumula Nelumbinis
  2. angiotensin II
  3. reactive oxygen species
  4. nuclear factor-κB
  5. fractalkine
  6. endothelial cells
Abstract(s)

Angiotensin II (Ang II) is a neuroendocrine factor that promotes hypertension and has been implicated in vascular inflammation through the induction of reactive oxygen species (ROS) and proinflammatory genes in endothelial cells. However, relatively little attention has been paid to the effect of Ang II on fractalkine (FKN), an important chemokine involved in endothelial dysfunction. In the study, we aimed to investigate the protective role of total flavonoids from Plumula Nelumbinis (TFPN), the main component extracted from Semen Nelumbinis, in Ang II-induced oxidative stress injury in human umbilical vein endothelial cells (HUVECs). Furthermore, we studied whether TFPN could attenuate the Ang II-induced generation of ROS and the activation of nuclear factor-κB (NF-κB); whether these Ang II-induced effects were inhibited by apocynin (a nicotinamide adenine dinucleotide phosphate oxidase inhibitor) and pyrrolidine dithiocarbamate (an NF-κB inhibitor). In the present study, it was observed that total flavonoids from Plumula Nelumbinis (TFPN), the main component extracted from Semen Nelumbinis, concentration-dependently inhibited the FKN production induced by Ang II in human umbilical vein endothelial cells (HUVECs). Furthermore, TFPN attenuated the Ang II-induced generation of ROS and the activation of nuclear factor-κB (NF-κB); these Ang II-induced effects were also inhibited by apocynin (a nicotinamide adenine dinucleotide phosphate oxidase inhibitor) and pyrrolidine dithiocarbamate (an NF-κB inhibitor). In conclusion, the findings of the present study indicate that TFPN attenuate Ang II-induced upregulation of FKN by inhibiting the ROS/NF-κB pathway in HUVECs and thus have a suppressive effect on vascular inflammation.