Triptolide attenuates lipopolysaccharide-induced inflammatory responses in human endothelial cells: involvement of NF-κB 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)-κB 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-κB p65 associated with attenuating IκBα phosphorylation and its degradation. Additionally, the present study revealed that triptolide inhibited LPS-triggered NF-κB 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-κB activation. Electronic supplementary material The online version of this article (10.1186/s12906-019-2616-3) contains supplementary material, which is available to authorized users.

Inhibition of JAK2/STAT3/SOCS3 signaling attenuates atherosclerosis in rabbit

“…2 The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China. 3 Beijing Information Science & Technology University, Beijing 100192, China.…”

“…Atherosclerosis, a complex cardiovascular disease, has been reported as a chronic inflammatory disease by the increasing studies [1,2]. At different stages of atherosclerosis, the infiltration of various inflammatory cells, such as T cells, mast cells and macrophages, into the atherosclerotic plaques is one of the main characteristics of atherosclerosis [3]. Subsequently, the migration and proliferation of vascular smooth muscle cells (VSMCs), which attribute to the formation of neointima and atherosclerotic plaques, could be promoted by these infiltrated inflammatory cells in company with the resident vascular wall cells via the secretion of cytokines and growth factors [4][5][6].…”

Salidroside protects endothelial cells against LPS-induced inflammatory injury by inhibiting NLRP3 and enhancing autophagy

“…It remains a great challenge to alleviate sepsis-induced endothelial injury. Moreover, recently some herbal medicines have been found to improve endothelial dysfunction and reduce inflammatory responses in LPS-induced HUVECs [8,9]. Therefore, more effective drugs are needed for protection against endothelial injury in sepsis.…”

Healing Effects of Single-Dose Triptolide in Rats with Severe Acute Pancreatitis

“…These properties of triptolide are explained by the inhibition of the production of cytokines such as TNF-alpha, IL-1, IL-6, IL-8 and phagocytosis of phagocytes. It has been shown that these effects of triptolide are closely related to NF-κB activity (7,8,20). Gray et al (21) reported that lung and liver damage occur due to the activation of NF-κB in the presence of pancreatitis-induced SIRS.…”

“…Triptolide is extracted from the roots of Chinese herb Tripterygium wilfordii and is known as an NF-κB inhibitor. Previous studies have shown that triptolide has a broad-spectrum therapeutic potential due to its immunosuppressive, anti-inflammatory and anti-tumor properties (6)(7)(8). Our experimental study aimed to investigate the healing effects of single dose-triptolide treatment in the early phase of cerulein-induced severe acute pancreatitis in rats.…”