PMID- 20332635
OWN - NLM
STAT- MEDLINE
DCOM- 20100621
LR  - 20190212
IS  - 1421-9778 (Electronic)
IS  - 1015-8987 (Linking)
VI  - 25
IP  - 4-5
DP  - 2010
TI  - Dehydroxymethylepoxyquinomicin inhibits expression and production of inflammatory 
      mediators in interleukin-1beta-induced human chondrocytes.
PG  - 543-50
LID - 10.1159/000303058 [doi]
AB  - The present research was carried out to determine the effects of a nuclear 
      factor-kappaB (NF-kappaB) inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), 
      derivative of the antibiotic epoxyquinomicin C, on normal human chondrocytes 
      treated with interleukin-1beta (IL-1beta). This is a cell model particularly 
      useful to reproduce the mechanisms involved in degenerative arthropathies, where 
      oxidative-inflammatory stress determines a progressive destruction of the 
      articular cartilaginous tissue. The expression of inducible nitric oxide synthase 
      (iNOS), cyclooxygenase-2 (COX-2), and inter-cellular adhesion molecule (ICAM)-1 
      was evaluated through Western blot analysis. The release of chemokines like 
      monocyte chemoattractant protein-1 (MCP-1), regulated upon normal activation 
      T-cell expressed and secreted (RANTES), and interleukin-8 (IL-8) were determined 
      by ELISA assays. DHMEQ acts as a potent inhibitor of iNOS and COX-2 gene 
      expression while also suppressing the production of nitrite in human 
      chondrocytes. In addition, DHMEQ induces a significant dose-dependent decrease in 
      ICAM expression, MCP-1, RANTES, and IL-8 release. DHMEQ helps to decrease the 
      expression and production of pro-inflammatory mediators in IL-1beta-induced 
      chondrocytes. DHMEQ may become a therapeutic agent for treatment of 
      chondro-degenerative diseases.
CI  - 2010 S. Karger AG, Basel.
FAU - Cardile, Venera
AU  - Cardile V
AD  - Department of Physiological Sciences, University of Catania, Catania, Italy. 
      cardile@unict.it
FAU - Frasca, Giuseppina
AU  - Frasca G
FAU - Libra, Massimo
AU  - Libra M
FAU - Caggia, Silvia
AU  - Caggia S
FAU - Umezawa, Kazuo
AU  - Umezawa K
FAU - Panico, Annamaria
AU  - Panico A
FAU - Malaponte, Grazia
AU  - Malaponte G
LA  - eng
PT  - Journal Article
DEP - 20100323
PL  - Germany
TA  - Cell Physiol Biochem
JT  - Cellular physiology and biochemistry : international journal of experimental 
      cellular physiology, biochemistry, and pharmacology
JID - 9113221
RN  - 0 (Benzamides)
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL5)
RN  - 0 (Cyclohexanones)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Interleukin-8)
RN  - 0 (Nitrates)
RN  - 0 (dehydroxymethylepoxyquinomicin)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - EC 1.14.13.39 (NOS2 protein, human)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
RN  - EC 1.14.99.1 (PTGS2 protein, human)
SB  - IM
MH  - Benzamides/*pharmacology
MH  - Cartilage, Articular/cytology
MH  - Cells, Cultured
MH  - Chemokine CCL2/metabolism
MH  - Chemokine CCL5/metabolism
MH  - Chondrocytes/drug effects/*metabolism
MH  - Cyclohexanones/*pharmacology
MH  - Cyclooxygenase 2/metabolism
MH  - Humans
MH  - Inflammation Mediators/*metabolism
MH  - Intercellular Adhesion Molecule-1/metabolism
MH  - Interleukin-1beta/*pharmacology
MH  - Interleukin-8/metabolism
MH  - Nitrates/metabolism
MH  - Nitric Oxide Synthase Type II/metabolism
EDAT- 2010/03/25 06:00
MHDA- 2010/06/22 06:00
CRDT- 2010/03/25 06:00
PHST- 2010/02/08 00:00 [accepted]
PHST- 2010/03/25 06:00 [entrez]
PHST- 2010/03/25 06:00 [pubmed]
PHST- 2010/06/22 06:00 [medline]
AID - 000303058 [pii]
AID - 10.1159/000303058 [doi]
PST - ppublish
SO  - Cell Physiol Biochem. 2010;25(4-5):543-50. doi: 10.1159/000303058. Epub 2010 Mar 
      23.