META060 attenuates TNF-α-activated inflammation, endothelial–monocyte interactions, and matrix metalloproteinase-9 expression, and inhibits NF-κB and AP-1 in THP-1 monocytes

Establishment of an interleukin-1β-induced inflammation-activated endothelial cell-smooth muscle cell-mononuclear cell co-culture model and evaluation of the anti-inflammatory effects of tanshinone IIA on atherosclerosis

“…Atherosclerosis is commonly understood as an inflammatory vascular disease, and targeting key inflammatory mediators through the inhibition of cytokine activities is a successful approach for preventing or slowing the progression of atherosclerosis (20). Previous studies have started to use inflammatory cytokines directly, as inflammatory inducers, to stimulate cells in the vascular wall to initiate the inflammatory process of atherosclerosis.…”

“…Previous studies have started to use inflammatory cytokines directly, as inflammatory inducers, to stimulate cells in the vascular wall to initiate the inflammatory process of atherosclerosis. This simulation may assist in evaluating drugs with potential anti-atherosclerotic and anti-inflammatory actions, with the most important stimulating factor being tumour necrosis factor (TNF)-α (20–22). In our previous study, we demonstrated that TNF-α exhibits a number of effects as a stimulator, however, TNF-α was not an ideal stimulator in this EC-SMC-MC model.…”

In vitro effect of caffeic acid phenethyl ester on matrix metalloproteinases (MMP-1 and MMP-9) and their inhibitor (TIMP-1) in lipopolysaccharide-activated human monocytes

“…[5][6][7] However, in recent years it has become evident that these enzymes also play a role in tissue degradation in different diseases such as cancer and chronic inflammatory processes. [6][7][8][9][10][11][12][13] The MMPs have been also associated with periodontitis and apical periodontitis in which bacteria and their components induce an inflammatory response that leads to the excessive production and the activation of these enzymes which, in turn, cause tissue destruction. [13][14][15][16] In addition, it is also known that an imbalance between MMP and tissue inhibitors of metalloproteinase (TIMP) is responsible for tissue degradation.…”

Genistein inhibits TNF-α-induced endothelial inflammation through the protein kinase pathway A and improves vascular inflammation in C57BL/6 mice

“…Although the pathogenesis of atherosclerotic vascular disease involves multifactorial processes, accumulating evidence demonstrates that inflammation and its subsequent endothelial dysfunction play a fundamental role in the initiation and progression of atherosclerosis [2]. The recruitment of monocytes by the activated endothelial cells (ECs) mediates the vascular inflammation and leads to the development of atherosclerosis [3]. Inflammation was reported to involve in the important stages of atherosclerosis such as adhesion and migration of monocytes into subendothelial space followed by the formation and rupture of atherosclerotic plaque [3].…”

“…The recruitment of monocytes by the activated endothelial cells (ECs) mediates the vascular inflammation and leads to the development of atherosclerosis [3]. Inflammation was reported to involve in the important stages of atherosclerosis such as adhesion and migration of monocytes into subendothelial space followed by the formation and rupture of atherosclerotic plaque [3]. It is now recognized that atherosclerosis is strongly modulated by pro-inflammatory mediators such as thrombin, tumor necrosis factor-alpha (TNF-α), and cell adhesion molecules secreted by injured ECs including monocyte chemoattractant protein-1 (MCP-1), vascular cell adhesion molecule-1 (VCAM-1), and intracellular adhesion molecule-1 (ICAM-1) [2, 4–6].…”