Terrein reduces pulpal inflammation in human dental pulp cells.
Terrein is a bioactive fungal metabolite whose anti-inflammatory properties are virtually unknown. The purpose of this study was to determine the effects of terrein on lipopolysaccharide (LPS)-induced expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in human dental pulp cells and to determine the mechanism of the observed effects. The LPS-induced expression of ICAM-1 and VCAM-1 was inhibited by terrein in both a time- and dose-dependent manner. LPS-stimulated translocation of nuclear factor kappa B (NF-kappaB) into the nucleus, which was blocked by inhibitors of amino kinase terminal (AKT, LY294002), extracellular signal regulated kinase 1/2 (ERK 1/2, PD98059), p38 (SB203580), and c-jun NH2-terminal kinase (JNK, SP600125) or terrein. In addition, these inhibitors and terrein also reduced the level of ICAM-1 and VCAM-1 expression in LPS-induced inflammation of pulp cells. Terrein suppressed NF-kappaB activation by blocking the activation of Akt. These results strongly suggest the potential role of terrein as an anti-inflammatory modulator in pulpal inflammation.
Lee
Jung-Chang
JC
Department of Oral Biochemistry, School of Dentistry, Chonbuk National University, Jeonbuk, Korea.
Yu
Mi-Kyung
MK
Lee
Rin
R
Lee
Young-Hee
YH
Jeon
Jae-Gyu
JG
Lee
Min-Ho
MH
Jhee
Eun-Chung
EC
Yoo
Ick-Dong
ID
Yi
Ho-Keun
HK
D021581:Active Transport, Cell Nucleus / Q000187:drug effects; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D003517:Cyclopentanes / Q000494:pharmacology / Q000627:therapeutic use*; D003782:Dental Pulp / Q000378:metabolism*; D004789:Enzyme Activation / Q000187:drug effects; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000096:biosynthesis; D008070:Lipopolysaccharides / Q000494:pharmacology; D020928:Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000378:metabolism; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D000081082:Phosphoinositide-3 Kinase Inhibitors; D010766:Phosphorylation; D011671:Pulpitis / Q000188:drug therapy* / Q000378:metabolism; D019010:Vascular Cell Adhesion Molecule-1 / Q000096:biosynthesis
D000894:Anti-Inflammatory Agents, Non-Steroidal; D003517:Cyclopentanes; D018799:Intercellular Adhesion Molecule-1; D008070:Lipopolysaccharides; D020928:Mitogen-Activated Protein Kinases; D016328:NF-kappa B; D019869:Phosphatidylinositol 3-Kinases; D000081082:Phosphoinositide-3 Kinase Inhibitors; D019010:Vascular Cell Adhesion Molecule-1; C439087:terrein