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KMID : 1161420150180090972
Journal of Medicinal Food
2015 Volume.18 No. 9 p.972 ~ p.979
Osthole Attenuates Inflammatory Responses and Regulates the Expression of Inflammatory Mediators in HepG2 Cells Grown in Differentiated Medium from 3T3-L1 Preadipocytes
Wu Shu-Ju

Abstract
This study explored the anti-inflammatory mechanisms by which osthole acted on HepG2 cells cultured in a differentiated medium from cultured 3T3-L1 preadipocyte cells. HepG2 cells, a human liver cell line, were treated with various concentrations of osthole in differentiated media from cultured 3T3-L1 cells to evaluate proinflammatory cytokines, inflammatory mediators, and signaling pathways. We used enzyme-linked immunosorbent assay kits to determine the levels of proinflammatory cytokines, real-time polymerase chain reaction to assay the mRNA expression, and western blot to determine the expression of cyclooxygenase-2 (COX-2) and heme oxygenase-1 (HO-1) proteins. We also investigated inflammatory mechanism pathway members, including mitogen-activated protein kinase (MAPK) and nuclear transcription factor kappa-B (NF-¥êB). Osthole was able to suppress the levels of proinflammatory cytokines interleukin (IL)-1¥â and IL-6, as well as chemokines monocyte chemoattractant protein-1 and IL-8. In addition, COX-2 was suppressed and HO-1 expression was increased in a concentration-dependent manner. Osthole was also able to decrease I¥êB-¥á phosphorylation and suppress the phosphorylation of MAPKs. These results suggest that osthole has anti-inflammatory effects as demonstrated by the decreased proinflammatory cytokine and mediator production through suppression of the NF-¥êB and MAPK signaling pathways in HepG2 cells when they are incubated on the differentiated medium from 3T3-L1 cells.
KEYWORD
HepG2, inflammation, MAPK, NF-¥êB, osthole
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