Adenophorae Radix Attenuates Mast Cell-mediated Allergic Inflammation through Down-regulation of NF-κB/ Caspase-1 Activation
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Adenophorae Radix (AR) has been used as a traditional medicine for various diseases. However, the regulatorymechanisms of AR in allergic inflammation are not yet understood. The present study was conducted to investigate theeffect and mechanisms of AR on the mast cell-mediated allergic response. To determine the pharmacological mechanismsof AR in allergic inflammation, we evaluated the effects of AR on the production of tumor necrosis factor (TNF)-α,interleukin (IL)-6, IL-1β and IL-8 as well as the activation of nuclear factor-κB (NF-κB) and caspase-1 in phorbol12-myristate 13-acetate plus calcium ionophore A23187 (PMACI)-stimulated human mast cells (HMC-1). Our resultsdemonstrated that AR effectively attenuated the PMACI-induced production of TNF-α, IL-6, IL-1β and IL-8 in stimulatedHMC-1. Additionally, we showed that the inhibitory effect of AR on inflammatory cytokines in PMACI-stimulated HMC-1cells involved the suppression of the activation NF-kB/caspase-1 in PMACI-stimulated HMC-1. Collectively, thesefindings provide experimental evidence that AR may be a useful candidate for the treatment of allergic inflammation.
Abstract
Adenophorae Radix (AR) has been used as a traditional medicine for various diseases. However, the regulatorymechanisms of AR in allergic inflammation are not yet understood. The present study was conducted to investigate theeffect and mechanisms of AR on the mast cell-mediated allergic response. To determine the pharmacological mechanismsof AR in allergic inflammation, we evaluated the effects of AR on the production of tumor necrosis factor (TNF)-α,interleukin (IL)-6, IL-1β and IL-8 as well as the activation of nuclear factor-κB (NF-κB) and caspase-1 in phorbol12-myristate 13-acetate plus calcium ionophore A23187 (PMACI)-stimulated human mast cells (HMC-1). Our resultsdemonstrated that AR effectively attenuated the PMACI-induced production of TNF-α, IL-6, IL-1β and IL-8 in stimulatedHMC-1. Additionally, we showed that the inhibitory effect of AR on inflammatory cytokines in PMACI-stimulated HMC-1cells involved the suppression of the activation NF-kB/caspase-1 in PMACI-stimulated HMC-1. Collectively, thesefindings provide experimental evidence that AR may be a useful candidate for the treatment of allergic inflammation.
참고문헌 (25)
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