BACKGROUND: Intestinal epithelial cells (IECs) can produce cytokines and chemokines that play an important role in the mucosal immune response. Regulation of this production is important to prevent inflammatory tissue damage. The root and stem barks of Acanthopanax species have been used as a tonic and sedative as well as in the treatment of rheumatism and diabetes. The aim of this study was to examine the inhibitory effect of acanthoic acid isolated from Acanthopanax koreanum (Araliaceae), on IL-8 production via mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-kappaB) in TNF-alpha-stimulated human colon epithelial cells. METHODS: HT29 cells were stimulated with TNF-alpha in the presence or absence of acanthoic acid. IL-8 production was measured by enzyme-linked immunosorbent assay (ELISA) and reverse transcription-PCR (RT-PCR). MAPK activation and IkappaB/NF-kappaB expression were assessed by Western blot analysis. NF-kappaB activation was determined using immunofluorescence localization and electrophoretic mobility shift assay (EMSA). RESULTS: Acanthoic acid suppressed TNF-alpha-induced IL-8 production in a dose-dependent manner. Furthermore, acanthoic acid inhibited TNF-alpha-induced MAPKs (p38, JNK1/2, and ERK1/2) activation, IkappaB degradation, NF-kappaB nuclear translocation, and NF-kappaB/DNA binding activity. CONCLUSION: Acanthoic acid might inhibit TNF-alpha-mediated IL-8 production by blocking in both the MAPKs and NF-kappaB pathways in HT29 cells.
BACKGROUND: Intestinal epithelial cells (IECs) can produce cytokines and chemokines that play an important role in the mucosal immune response. Regulation of this production is important to prevent inflammatory tissue damage. The root and stem barks of Acanthopanax species have been used as a tonic and sedative as well as in the treatment of rheumatism and diabetes. The aim of this study was to examine the inhibitory effect of acanthoic acid isolated from Acanthopanax koreanum (Araliaceae), on IL-8 production via mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-kappaB) in TNF-alpha-stimulated human colon epithelial cells. METHODS: HT29 cells were stimulated with TNF-alpha in the presence or absence of acanthoic acid. IL-8 production was measured by enzyme-linked immunosorbent assay (ELISA) and reverse transcription-PCR (RT-PCR). MAPK activation and IkappaB/NF-kappaB expression were assessed by Western blot analysis. NF-kappaB activation was determined using immunofluorescence localization and electrophoretic mobility shift assay (EMSA). RESULTS:Acanthoic acid suppressed TNF-alpha-induced IL-8 production in a dose-dependent manner. Furthermore, acanthoic acid inhibited TNF-alpha-induced MAPKs (p38, JNK1/2, and ERK1/2) activation, IkappaB degradation, NF-kappaB nuclear translocation, and NF-kappaB/DNA binding activity. CONCLUSION:Acanthoic acid might inhibit TNF-alpha-mediated IL-8 production by blocking in both the MAPKs and NF-kappaB pathways in HT29 cells.