Escin inhibits lipopolysaccharide-induced inflammation in human periodontal ligament cells

Abstract

Abstract. Periodontitis is a chronic inflammatory disease associated with gram-negative subgingival microflora infection. Accumulating experimental evidence suggests that escin exerts anti-inflammatory and anti-edematous effects. This study was designed to investigate the in vitro effects of escin on the inflammatory reaction of human periodontal ligament cells (hPDLs). hPDLs were stimulated with lipopolysaccharide (LPS). The cells were treated with various concentrations of escin. The viability of hPDLs was evaluated using the MTT method. The expression of Toll-like receptor 2 (TLR2) in hPDLs and the levels of IL-1β, TNF-α and IL-6 in the supernatant were measured. Escin significantly attenuated LPS-induced cytotoxicity in a concentration-dependent manner in hPDLs. Treatment with escin partly blocked the expression of TLR2. Escin also lowered the increase of proinflammatory cytokines (IL-1β, TNF-α and IL-6) induced by LPS. The present findings show that escin exerts a protective effect against LPS-induced inflammation in hPDLs. It was also shown that escin is a promising medicine for the treatment of periodontitis.

Virucidal, antiviral and immunomodulatory activities of β-escin and Aesculus hippocastanum extract

“…NF‐κB and AP‐1 activation following HSV infection is necessary for viral replication . Besides, the downregulation of NF‐κB activation by β‐escin has been described in different conditions . Therefore, we decided to investigate whether β‐escin and AH could exert their antiviral action through the inhibition of HSV‐1‐induced NF‐κB and AP‐1 activation.…”

“…Regarding the therapeutic significance and popularity of β‐escin, in the United States and Europe remains one of the best‐selling herbal products . With respect to its mechanism of anti‐inflammatory action, it has been reported that β‐escin inhibits NF‐κB activation in LPS‐treated mice and in several tumour cell types, macrophages and endothelial cells in vitro …”

Downregulation of tumor necrosis factor and other proinflammatory biomarkers by polyphenols

“…While 51 acute inflammation is therapeutic, chronic inflammation causes 52 numerous chronic diseases. At the molecular level, inflammation 53 is regulated by numerous molecules and factors, including cyto- 54 kines [interleukin (IL)-1, IL-2, IL-6, IL-12, tumor necrosis factor 55 (TNF)-a, TNF-b], 1 chemokines (monocyte chemoattractant protein 56 1, IL-8), proinflammatory transcription factors [nuclear factor- 57 kappaB (NF-jB), signal transducer and activator of transcription 58 (STAT)-3], proinflammatory enzymes [cyclooxygenase (COX)-2, 59 5-lipoxygenase (LOX), 12-LOX, matrix metalloproteinases (MMPs), 60 prostate-specific antigen (PSA), C-reactive protein, adhesion http 62 adhesion molecule (VCAM)-1, endothelial-leukocyte adhesion mole- 63 cule (ELAM)-1), vascular endothelial growth factor (VEGF), and 64 TWIST [1]. Among all these mediators, NF-jB is the central regulator 65 of inflammation [1,2].…”

“…Lowered LPS-induced TNF-a, IL-1b, and IL-6 levels in human periodontal ligament cells [59]. Inhibited secretion of TNF-a, NO, and IL-1b in LPS-stimulated RAW macrophages [142].…”

Anti-inflammatory and Anti-cancer Properties of β-Escin, a Triterpene Saponin

“…β-Escin dose-dependently enhanced hypoxiainduced activation of human endothelial cells and caused inhibition of phospholipase A2, an enzyme responsible for the release of precursors of inflammatory mediators [60]. Recently, Liu et al [61] observed the in vitro effects of escin on the inflammatory reaction of human periodontal ligament cells, finding a significant blockade of the expression of Toll-like receptor (TLR)2 and decreased pro-inflammatory cytokines interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and IL-6 induced by lipopolysaccharide (LPS; 62). A recent study showed that escin has a potent protective effect on LPS-induced acute lung injury by inhibiting the inflammatory response [62].…”