Anti-inflammatory functions of purpurogallin in LPS-activated human endothelial cells

Abstract

Enzymatic oxidation of commercially available pyrogallol was efficiently transformed to an oxidative product, purpurogallin. Purpurogallin plays an important role in inhibiting glutathione S-transferase, xanthine oxidase, catechol O-methyltransferase activities and is effective in the cell protection of several cell types. However, the anti-inflammatory functions of purpurogallin are not well studied. Here, we determined the effects of purpurogallin on lipopolysaccharide (LPS)-mediated proinflammatory responses. The results showed that purpurogallin inhibited LPS-mediated barrier hyper-permeability, monocyte adhesion and migration and such inhibitory effects were significantly correlated with the inhibitory functions of purpurogallin on LPS-mediated cell adhesion molecules (vascular cell adhesion molecules, intracellular cell adhesion molecule, E-selectin). Furthermore, LPS-mediated nuclear factor-κB (NF-κB) and tumor necrosis factor-α (TNF-α) releases from HUVECs were inhibited by purpurogallin. Given these results, purpurogallin showed its anti-inflammatory activities and could be a candidate as a therapeutic agent for various systemic inflammatory diseases. [BMB reports 2012; 45(3): [200][201][202][203][204][205]

Potential Herbal Therapy of HMGB1-Targeting Agent in Sepsis

“…(1) Herbal compounds could inhibit the binding and interactions of HMGB1 to its receptors. This concept was supported by the finding that herbal medicine blocks chemokine binding to its receptors [8][9][10][11][12][13][14]. (2) Herbal compounds could block the downstream signaling pathway of receptors activation by HMGB1; this is also supported by the finding that recently we showed that herbal compounds inhibited LPS-stimulated NF-κB activation which is the down-stream transcriptional factor of HMGB1 [8,11,[13][14][15][16][18][19][20][21][22].…”

“…We recently showed that herbal single compound down-regulated the cell surface expression of the three receptors, TLR-2, TLR-4, and RAGE, which are known to bind HMGB1 to initiate pro-inflammatory responses in endothelial cells [8][9][10][11][12][13][14]. Similar to HMGB1, LPS also upregulated the expression of all three receptors on endothelial cells, and single compound from herbal medicines down regulated this effect [8][9][10][11][12][13][14][15][16][17][18], suggesting that herbal compounds can inhibit the amplification of pro-inflammatory pathways propagated by LPS and HMGB1 during infections. There are several potential mechanisms by which herbal compounds could interfere with HMGB1 functions.…”

Ameliorative Effect of Vicenin-2 and Scolymoside on TGFBIp-Induced Septic Responses

“…Expression of vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and E-selectin on HUVECs was determined by whole-cell ELISA, as described previously [7,24]. Briefly, confluent monolayers of HUVECs were treated with TGFBIp (5 μg/ mL) for 6 h followed by each compound (20 μM) for another 6 h. The medium was removed, and cells were washed with PBS and fixed with 50 μL of 1 % paraformaldehyde for 15 min at room temperature.…”

Inhibitory effects of polyozellin from Polyozellus multiplex on HMGB1-mediated septic responses

“…Expressions of vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and E-selectin on HUVECs were determined by whole-cell ELISA, as described in previous studies [39,40]. Briefly, confluent monolayers of HUVECs were treated with HMGB1 (1 lg/mL) for 16 h followed by polyozellin (0-20 lM) for 6 h. The medium was then removed, and the cells were washed with PBS and fixed with 50 lL of 1 % paraformaldehyde for 15 min at room temperature.…”