Triptolide attenuates lipopolysaccharide-induced inflammatory responses in human endothelial cells: involvement of NF-?B pathway.

ABSTRACT:

Background

Endothelial cell inflammation is a central event in the pathogenesis of numerous cardiovascular diseases, including sepsis and atherosclerosis. Triptolide, a principal bioactive ingredient of Traditional Chinese Medicine Tripterygium wilfordii Hook.F., displays anti-inflammatory actions in vivo. However, the mechanisms underlying these beneficial effects remain undetermined. The present study investigated the effects and possible mechanisms of triptolide on lipopolysaccharide (LPS)-induced inflammatory responses in human umbilical vein endothelial cells (HUVECs).

Methods

The effects of triptolide on the LPS-induced production and expression of inflammatory molecules, monocyte adhesion and activation of nuclear factor (NF)-?B pathway were examined in cultured HUVECs.

Results

In cultured HUVECs, pre-treatment with triptolide dose-dependently attenuated LPS-induced cytokine and chemokine production, adhesion molecule expression and monocyte adhesion. Mechanistically, triptolide was found to dose-dependently inhibit the LPS-induced increases in the DNA binding activity of NF-?B p65 associated with attenuating I?B? phosphorylation and its degradation. Additionally, the present study revealed that triptolide inhibited LPS-triggered NF-?B transcriptional activation in a dose-dependent manner.

Conclusions

The results of the present study indicated that triptolide suppresses the inflammatory response of endothelial cells possibly via inhibition of NF-?B activation.

SUBMITTER: Song C 

PROVIDER: S-EPMC6679459 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature