Opuntia ficus-indica (OFI), or Pricky Pear Cactus, is effective in cough, fever, pain and anti-inflammatory action, and asthma. This study aims to investigate the effect of OFI stem extract on the respiratory system of animal models induced by ovalbumin (OVA) and fine dust (PM10) and to analyze the indicator substances of OFI stem extract. In the OFI stem 50% ethanol extract (OFI-50E) administration group, the number of immune cells and inflammatory cytokines in the lungs and BAL decreased to a similar level to the positive control group administered with dexamethasone. In addition, OVA-specific IgE and airway hyper-reactivity (AHR) were significantly reduced. Also, the deposition of PM10 observed through staining of lung tissue was clearly reduced in the OFI-50E 200 mg/kg administration group. The anti-inflammatory mechanism in the lung was found to obstruct the production of inflammatory cytokines by impeding the NF-kB and MAPK pathways through the inhibition of IRAK-1 active cells. The main component of OFI stem 50% ethanol extract was identified to be narcissin. According to the study results, OFI is expected to be a respiratory health functional food.

Background: Small particles increase airway inflammation upon reaching the alveoli. Here, we investigated the protective or therapeutic effects of Salvia plebeia R. Br. (SP_R) extracts on airway inflammation. Methods and Results: To investigate the anti-inflammatory activity of SP_R extracts, we measured their inhibitory effect on the production of reactive oxygen species (ROS) expression of inflammatory mediators, and immune cell infiltration in MH-S alveolar macrophage cells and in the ambient particulate matter (APM)-exposed airway inflammation mice model. The SP_R extracts inhibited the production of ROS and expression of IL-4, IL-10, IL-15, and IL-17A mRNA in APM-stimulated MH-S cells. Oral administration of SP_R extracts suppressed APM-induced inflammatory symptoms, such as high alveolar wall thickness, excess collagen fibers, decreased mRNA expression of chemokines (Ccr9, Ccl5, Ccr3), inflammatory cytokines (IL-15, TNF-α), and IL-4 Th2 cytokine in the lung. The SP_R extracts also inhibited ROS production, granulocyte (CD11b+Gr-1+) infiltration, IL-17A, TNF-α, macrophage inflammatory protein (Mip-2), and chemokine (C-X-C motif) ligand 1 (Cxcl-1) production in the airway. The specific compounds in the SR-R extracts that mediate the anti-inflammatory effects were identified. Conclusions: In this study, SP_R extracts effectively inhibited airway inflammatory responses, such as ROS production and granulocyte infiltration into the airway, by regulating the expression of chemokines and inflammatory cytokines.