Nuclear factor kappaB-mediated down-regulation of adhesion molecules: Possible mechanism for inhibitory activity of bigelovin against inflammatory monocytes adhesion to endothelial cells

Nam, Kung Woo; Oh, Goo Taeg; Seo, Eun Kyoung; Kim, Kyeong Ho; Koo, Uk; Lee, Sung‐Jin; Mar, Woongchon

doi:10.1016/j.jep.2009.03.017

Cited by 16 publications

(13 citation statements)

References 31 publications

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“…To date, various sesquiterpenes have been isolated from I. japonica and their biological activities have been evaluated. For example, the sesquiterpenes lactone ergolide, eupatolide, and 1-O-acetylbritanni- lactone suppress the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) by inhibiting nuclear translocation of nuclear factor-κB (NF-κB) activation [22][23][24], and bigelovin inhibits inflammatory monocyte adhesion to endothelial cells [25]. Furthermore, ergolide causes the induction of apoptosis in Jurkat T cells [26], and eupatolide can augment apoptosis in human breast cancer cells [27], while 1-O-acetylbritannilactone induces the occurrence of apoptosis in HL-60 cells [28] and suppresses abnormal vascular smooth muscle cell proliferation [29].…”

Section: Resultsmentioning

confidence: 99%

Anti-inflammatory Terpenes from Flowers of Inula japonica

et al. 2014

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Section: Resultsmentioning

confidence: 99%

Anti-inflammatory Terpenes from Flowers of Inula japonica

et al. 2014

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“…It has been reported that bigelovin could also target the NF-κB and RXR pathways and trigger the proteolysis of E2F1 [41][42][43] . These targets are all relevant to cancer cell survival and growth.…”

Section: Discussionmentioning

confidence: 99%

Bigelovin inhibits STAT3 signaling by inactivating JAK2 and induces apoptosis in human cancer cells

et al. 2015

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Aim: To study the function and mechanism of bigelovin, a sesquiterpene lactone from the flower of Chinese herb Inula hupehensis, in regulating JAK2/STAT3 signaling and cancer cell growth. Methods: HepG2 cells stably transfected with the STAT3-responsive firefly luciferase reporter plasmid (HepG2/STAT3 cells), and a panel of human cancer cell lines were used to identify active compounds. Cell viability was measured using MTT assay. Western blotting was used to detect protein expression and phosphorylation. Kinase assays were performed and the reaction between bigelovin and thiolcontaining compounds was analyzed with LC-MS.

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“…Cell-surface adhesion molecules like E-selectin and ICAM-1 are released on endothelial cell activation and are responsible for the recruitment of various leukocytes leading to an increase in endothelial permeability and tissue damage [Cybulsky and Gimbrone, 1991;Frank and Lisanti, 2008;Nam et al, 2009]. Multiple factors can stimulate adhesion molecule expression in endothelial cells, of which LPS, the major cell wall component of the Gram-negative bacteria, is an important stimulus in infectious inflammation.…”

Section: Discussionmentioning

confidence: 99%

Peoniflorin prevents the adhesion between inflammatory endothelial cells and leukocytes through inhibiting the activation of MAPKs and NF‐κB

Gao

Song

et al. 2010

Drug Development Research

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The vascular endothelium can be activated by multiple factors, including lipopolysaccharide (LPS) functioning as a key component of the inflammatory response. Activated endothelium promotes the recruitment of leukocytes mainly by releasing various adhesion molecules and amplifies inflammation via a feedback loop. Peoniflorin, the main active constituent of the roots of Paeonia lactiora Pall., possesses anti-inammatory, anti-infective, and anti-platelet aggregative properties. To elucidate the anti-inammatory mechanism of peoniflorin, the present study was conducted to address its effects on the adhesion of inflammatory endothelial cells to leukocytes. Peoniflorin substantially reduced adhesion of either human acute monocytic leukemia cells (THP-1) or human acute promyelocytic leukemia cells (HL-60) to LPS-stimulated human umbilical vein endothelial cells (HUVECs). It also markedly down-regulated the expression of E-selectin at both the gene and protein levels. However, peoniflorin only slightly reduced expression of intercellular adhesion molecule-1 (ICAM-1). Signal pathway analysis indicated that peoniflorin reduced phosphorylation of c-Jun NH 2 -terminal kinase (JNK) and p38 kinase, as well as the phosphorylation and degradation of IkB-a in HUVECs. These findings suggest that prevention of the adhesion between inflammatory endothelial cells and leukocytes contributes, at least partially, to the anti-inflammation action of peoniflorin. The anti-adhesion Abbreviations used: LPS, lipopolysaccharide; GPL, glycosides isolated from the roots of Paeonia lactiora Pall.; HUVECs, human umbilical vein endothelial cells; HL-60, human acute promyelocytic leukemia cell line; THP-1, human acute monocytic leukemia cell line; MAPK, mitogen-activated protein kinase; JNK, c-Jun NH 2 -terminal kinase; ERK, extracellular signal-regulated kinase; NF-kB, nuclear factor-kappa B; ICAM-1, intercellular adhesion molecule-1; BCECF-AM, Bis-carboxyethyl-carboxyfluorescein acetoxy-methyl; DEX, dexamethasone; NBCS, newborn calf serum; TLR4, toll-like receptor 4; MD2, myeloid differentiation protein-2; IkB, inhibitor of kB.c 2010 Wiley-Liss, Inc.mechanisms of peoniflorin were involved in the down-regulation of the activation of mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-kB), and a reduction of adhesion molecule expressions in endothelial cells. Drug Dev Res 71: 275-284, 2010.

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Nuclear factor kappaB-mediated down-regulation of adhesion molecules: Possible mechanism for inhibitory activity of bigelovin against inflammatory monocytes adhesion to endothelial cells

Cited by 16 publications

References 31 publications

Anti-inflammatory Terpenes from Flowers of Inula japonica

Anti-inflammatory Terpenes from Flowers of Inula japonica

Bigelovin inhibits STAT3 signaling by inactivating JAK2 and induces apoptosis in human cancer cells

Peoniflorin prevents the adhesion between inflammatory endothelial cells and leukocytes through inhibiting the activation of MAPKs and NF‐κB

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