Aloin Inhibits Interleukin (IL)-1β−Stimulated IL-8 Production in KB Cells

• Hee Sam Na ^[1] ; Yu Ri Song ^[1] ; Seyeon Kim ^[1] ; Jun-Young Heo ; Hae-Young Chung ; Jin Chung ^[1]
  1. [1] Pusan National University

     Pusan National University

     Corea del Sur

     
• Localización: Journal of periodontology, ISSN 0022-3492, Vol. 87, Nº. 6, 2016, págs. 108-115
• Idioma: inglés
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• Resumen

  • Background: Interleukin (IL)-1β, which is elevated in oral diseases including gingivitis, stimulates epithelial cells to produce IL-8 and perpetuate inflammatory responses. This study investigates stimulatory effects of salivary IL-1β in IL-8 production and determines if aloin inhibits IL-1β−stimulated IL-8 production in epithelial cells.

    Methods: Saliva was collected from volunteers to determine IL-1β and IL-8 levels. Samples from volunteers were divided into two groups: those with low and those with high IL-1β levels. KB cells were stimulated with IL-1β or saliva with or without IL-1 receptor agonist or specific mitogen-activated protein kinase (MAPK) inhibitors. IL-8 production was measured by enzyme-linked immunosorbent assay (ELISA). MAPK protein expression involved in IL-1β−induced IL-8 secretion was detected by Western blot. KB cells were pretreated with aloin, and its effect on IL-1β−induced IL-8 production was examined by ELISA and Western blot analysis.

    Results: Saliva with high IL-1β strongly stimulated IL-8 production in KB cells, and IL-1 receptor agonist significantly inhibited IL-8 production. Low IL-1β–containing saliva did not increase IL-8 production. IL-1β treatment of KB cells induced activation of MAPK signaling molecules as well as nuclear factor-kappa B. IL-1β−induced IL-8 production was decreased by p38 and extracellular signal-regulated kinase (ERK) inhibitor treatment. Aloin pretreatment inhibited IL-1β−induced IL-8 production in a dose-dependent manner and inhibited activation of the p38 and ERK signaling pathway. Finally, aloin pretreatment also inhibited saliva-induced IL-8 production.

    Conclusions: Results indicated that IL-1β in saliva stimulates epithelial cells to produce IL-8 and that aloin effectively inhibits salivary IL-1β–induced IL-8 production by mitigating the p38 and ERK pathway. Therefore, aloin may be a good candidate for modulating oral inflammatory diseases.