Abstract
Interleukin-1β (IL-1β)-induced macrophage inflammatory protein-1β (MIP-1β) expression in hepatic cells has been found to contribute to several liver-related inflammatory diseases. The detail mechanism underlying IL-1β-mediated MIP-1β expression is still unclear. HE-145 is a natural product isolated from Taiwania cryptomerioides Hayata which posses antiviral activity against hepatitis B virus in human hepatoma cells. Recently, we found that HE-145 showed the suppressive effects on IL-1-β induced chemokine CC motif ligand 4 (CCL4) expression in Huh7 cells. Therefore, the molecular mechanism of IL-1β-mediated MIP-1β regulation is interested and the effects of HE-145 on MIP-1β expression were evaluated. Using mitogen-activated protein kinase (MAPK) inhibitors, HE-145 specifically inhibited IL-1β-induced c-Jun NH2 terminal kinase (JNK) signaling pathway. HE-145 suppressed the protein level of phosphor-c-Jun and had no suppressive effect on IL-1β-induced p38 signaling. In JNK kinase activity assay, HE-145 did not block JNK kinase activity. Furthermore, HE-145 did not suppress the complexes which are associated with JNK, c-Jun, and ATP at the activation of JNK. This selectively suppressive effect of HE-145 is direct neither to act with JNK nor the JNK/c-Jun complexes. Based on the anti-inflammatory effects of HE-145, HE-145 may be developed for treatment of liver inflammatory diseases.
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