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

• Published in: Journal of periodontology (1970) 2016-06, Vol.87 (6), p.e108-e115
• Main Authors: Na, Hee Sam, Song, Yu Ri, Kim, Seyeon, Heo, Jun‐Young, Chung, Hae‐Young, Chung, Jin
• Format: Article
• Language: English
• Subjects: Aloe; Cells, Cultured; Dentistry; Emodin - analogs & derivatives; Emodin - pharmacology; epithelial cells; Humans; Interleukin-1beta - physiology; Interleukin-6 - physiology; Interleukin-8 - metabolism; interleukin‐1beta; interleukin‐8; KB cells; KB Cells - metabolism; Mouth Diseases - metabolism; p38 Mitogen-Activated Protein Kinases
• ISSN: 0022-3492; 1943-3670
• DOI: 10.1902/jop.2016.150447

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.