Byakangelicol, isolated from Angelica dahurica, inhibits both the activity and induction of cyclooxygenase-2 in human pulmonary epithelial cells

C. H. Lin, C. W. Chang, C. C. Wang, M. S. Chang, L. L. Yang

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

We examined the inhibitory mechanism of byakangelicol, isolated from Angelica dahurica, on interleukin-1β (IL-1β)-induced cyclooxygenase-2 (COX-2) expression and prostaglandin E2 (PGE2) release in human pulmonary epithelial cell line (A549). Byakangelicol (10-50 μM) concentration-dependently attenuated IL-1β-induced COX-2 expression and PGE2 release. The selective COX-2 inhibitor, NS-398 (0.01-1 μM), and byakangelicol (10-50 μM) both concentration-dependently inhibited the activity of the COX-2 enzyme. Byakangelicol, at a concentration up to 200 μM, did not affect the activity and expression of COX-1 enzyme. IL-1β-induced p44/42 mitogen-activated protein kinase (MAPK) activation was inhibited by the MAPK/extracellular signal-regulated protein kinase (MEK) inhibitor, PD 98059 (30 μM), while byakangelicol (50 μM) had no effect. Treatment of cells with byakangelicol (50 μM) or pyrrolidine dithiocarbamate (PDTC; 50 μM) partially inhibited IL-1β-induced degradation of IκB-α in the cytosol, translocation of p65 NF-κB from the cytosol to the nucleus and the NF-κB-specific DNA-protein complex formation. Taken together, we have demonstrated that byakangelicol inhibits IL-1β-induced PGE2 release in A549 cells; this inhibition may be mediated by suppression of COX-2 expression and the activity of COX-2 enzyme. The inhibitory mechanism of byakangelicol on IL-1β-induced COX-2 expression may be, at least in part through suppression of NF-κB activity. Therefore, byakangelicol may have therapeutic potential as an anti-inflammatory drug on airway inflammation.

Original languageEnglish
Pages (from-to)1271-1278
Number of pages8
JournalJournal of Pharmacy and Pharmacology
Volume54
Issue number9
DOIs
Publication statusPublished - Sep 2002

Fingerprint

Angelica
Cyclooxygenase 2
Epithelial Cells
Interleukin-1
Lung
Dinoprostone
Mitogen-Activated Protein Kinases
Cytosol
Enzymes
byakangelicol
Cyclooxygenase 2 Inhibitors
Mitogen-Activated Protein Kinase Kinases
Extracellular Signal-Regulated MAP Kinases
Protein Kinase Inhibitors
Anti-Inflammatory Agents
Inflammation

ASJC Scopus subject areas

  • Pharmacology
  • Pharmaceutical Science

Cite this

Byakangelicol, isolated from Angelica dahurica, inhibits both the activity and induction of cyclooxygenase-2 in human pulmonary epithelial cells. / Lin, C. H.; Chang, C. W.; Wang, C. C.; Chang, M. S.; Yang, L. L.

In: Journal of Pharmacy and Pharmacology, Vol. 54, No. 9, 09.2002, p. 1271-1278.

Research output: Contribution to journalArticle

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abstract = "We examined the inhibitory mechanism of byakangelicol, isolated from Angelica dahurica, on interleukin-1β (IL-1β)-induced cyclooxygenase-2 (COX-2) expression and prostaglandin E2 (PGE2) release in human pulmonary epithelial cell line (A549). Byakangelicol (10-50 μM) concentration-dependently attenuated IL-1β-induced COX-2 expression and PGE2 release. The selective COX-2 inhibitor, NS-398 (0.01-1 μM), and byakangelicol (10-50 μM) both concentration-dependently inhibited the activity of the COX-2 enzyme. Byakangelicol, at a concentration up to 200 μM, did not affect the activity and expression of COX-1 enzyme. IL-1β-induced p44/42 mitogen-activated protein kinase (MAPK) activation was inhibited by the MAPK/extracellular signal-regulated protein kinase (MEK) inhibitor, PD 98059 (30 μM), while byakangelicol (50 μM) had no effect. Treatment of cells with byakangelicol (50 μM) or pyrrolidine dithiocarbamate (PDTC; 50 μM) partially inhibited IL-1β-induced degradation of IκB-α in the cytosol, translocation of p65 NF-κB from the cytosol to the nucleus and the NF-κB-specific DNA-protein complex formation. Taken together, we have demonstrated that byakangelicol inhibits IL-1β-induced PGE2 release in A549 cells; this inhibition may be mediated by suppression of COX-2 expression and the activity of COX-2 enzyme. The inhibitory mechanism of byakangelicol on IL-1β-induced COX-2 expression may be, at least in part through suppression of NF-κB activity. Therefore, byakangelicol may have therapeutic potential as an anti-inflammatory drug on airway inflammation.",
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AB - We examined the inhibitory mechanism of byakangelicol, isolated from Angelica dahurica, on interleukin-1β (IL-1β)-induced cyclooxygenase-2 (COX-2) expression and prostaglandin E2 (PGE2) release in human pulmonary epithelial cell line (A549). Byakangelicol (10-50 μM) concentration-dependently attenuated IL-1β-induced COX-2 expression and PGE2 release. The selective COX-2 inhibitor, NS-398 (0.01-1 μM), and byakangelicol (10-50 μM) both concentration-dependently inhibited the activity of the COX-2 enzyme. Byakangelicol, at a concentration up to 200 μM, did not affect the activity and expression of COX-1 enzyme. IL-1β-induced p44/42 mitogen-activated protein kinase (MAPK) activation was inhibited by the MAPK/extracellular signal-regulated protein kinase (MEK) inhibitor, PD 98059 (30 μM), while byakangelicol (50 μM) had no effect. Treatment of cells with byakangelicol (50 μM) or pyrrolidine dithiocarbamate (PDTC; 50 μM) partially inhibited IL-1β-induced degradation of IκB-α in the cytosol, translocation of p65 NF-κB from the cytosol to the nucleus and the NF-κB-specific DNA-protein complex formation. Taken together, we have demonstrated that byakangelicol inhibits IL-1β-induced PGE2 release in A549 cells; this inhibition may be mediated by suppression of COX-2 expression and the activity of COX-2 enzyme. The inhibitory mechanism of byakangelicol on IL-1β-induced COX-2 expression may be, at least in part through suppression of NF-κB activity. Therefore, byakangelicol may have therapeutic potential as an anti-inflammatory drug on airway inflammation.

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