Lipopolysaccharide-stimulated activation of murine DC2.4 cells is attenuated by n-butylidenephthalide through suppression of the NF-κB pathway

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Abstract
Modulation of dendritic cell (DC) fate and function may be one approach for the treatment of inflammatory and autoimmune diseases. n-Butylidenephthalide (BP), derived from Angelica sinensis, at 40 μg/ml significantly decreased the secretion of interleukin-6 and tumor necrosis factor-α by lipopolysaccharide (LPS)-stimulated activation of cultured murine DC2.4 cells (P < 0.01). LPS-induced major histocompatibility complex class II (P < 0.05), CD86 (P < 0.01) and CD40 (P < 0.01) expression on DC2.4 cells was also inhibited by BP. The endocytic capacity of LPS-stimulated DC2.4 cells was increased by BP (P < 0.01). The antigen-presenting capacity of LPS-stimulated DC2.4 cells was decreased by BP (P < 0.05). Moreover, we confirmed BP attenuates the responses of LPS-stimulated activation of DCs via suppression of NF-κB-dependent pathways.

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