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A Natural Lignan, HE‐145 Suppresses IL‐1 β induced MIP‐1 β Expression in Huh7 Cells
Author(s) -
Yeh Sheau Farn,
Tseng Pei Chi
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.lb15-a
Subject(s) - p38 mitogen activated protein kinases , chemokine , kinase , mapk/erk pathway , protein kinase a , chemistry , microbiology and biotechnology , signal transduction , mitogen activated protein kinase , biology , receptor , biochemistry
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 T aiwania 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.