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• W2511948238 abstract "ACTG-toxin H (AH) originates from Alternaria sp. In this study, we explored the molecular mechanism underlying the anti-inflammatory properties of AH. Treat- ment with AH inhibited lipopolysaccharide (LPS)-induced interleukin-6, IL-1b, inducible nitric oxide synthase, and cyclooxygenase-2 expression and nitric oxide production. Furthermore, AH inhibited LPS-induced P38 MAPK and Akt activation in RAW264.7 cells. Electrophoretic mobility shift assays (EMSAs) showed that AH inhibited LPS- induced nuclear factor-jB (NFjB) DNA-binding activity. Using transfection assay and measurement of an NFjB- sensitive promoter region, we found that transfection of toll- like receptor 4 (TLR4) increased LPS-induced NFjB tran- scription activity in 293T cells. AH significantly blocked LPS-induced NFjB activation in TLR4-transfected cells. Taken together, our data indicated that anti-inflammatory properties of AH resulted from the inhibition of proinflammatory cytokines and enzyme production via the TLR4/NFjB signaling pathway." @default.
• W2511948238 created "2016-09-16" @default.
• W2511948238 creator A5029397994 @default.
• W2511948238 creator A5065824261 @default.
• W2511948238 date "2013-01-01" @default.
• W2511948238 modified "2023-09-24" @default.
• W2511948238 title "Toll-like receptor 4/nuclear factor-jB signaling pathway is involved in ACTG-toxin H-mediated anti-inflammatory effect" @default.
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• W2511948238 hasPublicationYear "2013" @default.
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