Anti-inflammatory activity of c(ILDV-NH(CH2
)5
CO), a novel, selective, cyclic peptide inhibitor of VLA-4-mediated cell adhesion

Chalcone or (E)-1,3-diphenyl-2-propene-1-one scaffold has gained considerable scientific interest in medicinal chemistry owing to its simple chemistry, ease in synthesizing a variety of derivatives and exhibiting a broad range of promising pharmacological activities by modulating several molecular targets. A number of natural and (semi-) synthetic chalcone derivatives have demonstrated admirable anti-inflammatory activity due to their inhibitory potential against various therapeutic targets like Cyclooxygenase (COX), Lipooxygenase (LOX), Interleukins (IL), Prostaglandins (PGs), Nitric Oxide Synthase (NOS), Leukotriene D4 (LTD4), Nuclear Factor-κB (NF- κB), Intracellular Cell Adhesion Molecule-1 (ICAM-1), Vascular Cell Adhesion Molecule-1 (VCAM-1), Monocyte Chemoattractant Protein-1 (MCP-1) and TLR4/MD-2, etc. The chalcone scaffold with hydroxyl, methoxyl, carboxyl, prenyl group and/or heterocyclic ring substitution like thiophene/furan/indole showed promising anti-inflammatory activity. In this review, a comprehensive study (from the year 1991 to 2016) on multi-targets of inflammatory interest, related inflammation reactions and their treatment by chalcone-based inhibitors acting on various molecular targets entailed in inflammation, Structure-Activity Relationships (SARs), Mechanism of Actions (MOAs), and patents are highlighted.

Download Full-text

Anti-inflammatory and Antioxidant Effects of Pluchea indica Leaf Extract in TNF-α-Induced Human Endothelial Cells

Walailak Journal of Science and Technology (WJST) ◽

10.48048/wjst.2021.10271 ◽

2021 ◽

Vol 18 (10) ◽

Author(s):

Klaokwan SRISOOK ◽

Suthasinee JINDA ◽

Ekaruth SRISOOK

Keyword(s):

Endothelial Cells ◽

Cell Adhesion ◽

Leaf Extract ◽

Vascular Endothelial Cells ◽

Inflammatory Activity ◽

Dependent Manner ◽

Vascular Endothelial ◽

Herbal Tea ◽

Tnf Α ◽

Anti Inflammatory

Pluchea indica is a shrub plant found in mangrove forests. The leaves are consumed as food and herbal tea and exhibit various biological effects, such as antioxidant and anti-inflammatory activities, in macrophages and animal models. However, the inhibitory activity of P. indica leaf extract on vascular inflammation remains unknown. Therefore, this study investigated the effect of an ethanol extract from P. indica herbal tea leaves (PIE) on tumor necrosis factor-α (TNF-α)-induced human vascular endothelial EA.hy926 cells. The cytotoxic effect of PIE was determined by thiazolyl blue tetrazolium bromide assays. PIE at concentrations of 12.5 - 50 µg/mL did not show significant cytotoxicity, whereas PIE at concentrations ≥ 100 µg/mL decreased cell viability. PIE inhibited the production of reactive oxygen species (ROS) in TNF-α-stimulated endothelial cells. To evaluate the PIE’s anti-vascular inflammatory activity, the protein expression of cell adhesion molecules, including intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), was determined by western blot. PIE significantly decreased TNF-α-induced ICAM-1 and VCAM-1 expression in a concentration-dependent manner. Furthermore, PIE upregulated heme oxygenase-1 (HO-1) in a concentration- and time-dependent manner. Inhibiting the activity of HO-1 by tin protoporphyrin IX significantly blocked the suppressive effect of PIE on ICAM-1 but not VCAM-1 expression. Therefore, PIE exerts anti-inflammatory activity on vascular endothelial cells, at least in part, by suppressing ROS production and the induction of HO-1. The obtained data suggest that PIE is a promising substance for developing therapeutic agents or as an ingredient of functional food. HIGHLIGHTS Pluchea indica leaf extract (PIE) at non-toxic doses inhibited ICAM-1 and VCAM-1 in TNF-α-induced human vascular endothelial cells PIE suppressed the production of ROS in TNF-α-stimulated endothelial cells PIE exerts anti-inflammatory activity on vascular endothelial cells mediated partly through the upregulation of HO-1

Download Full-text