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Root Extract Ameliorates Ovalbumin-Induced Airway Inflammation in a CARAS Mouse Model by Modulating the IL-33/TSLP/NF-κB Signaling Pathway. | LitMetric

AI Article Synopsis

  • Asian knotweed's root extract (FJE) was tested for its effects on airway inflammation linked to combined allergic rhinitis and asthma (CARAS) in a mouse model.
  • Mice treated with FJE showed a decrease in allergic responses, including lower levels of IgE and inflammatory cytokines, while enhancing IgG2a levels.
  • FJE also improved histopathological conditions in nasal and lung tissues and influenced the IL-33/TSLP/NF-kB signaling pathway, suggesting its potential as a therapeutic for CARAS.

Article Abstract

(Asian knotweed) is a medicinal herb traditionally used to treat inflammation, among other conditions. However, the effects of root extract (FJE) on airway inflammation associated with combined allergic rhinitis and asthma (CARAS) and the related mechanisms have not been investigated. This study examined the effect of FJE against CARAS in an ovalbumin (OVA)-induced CARAS mouse model. Six-week-old male BALB/c mice were randomly segregated into six groups. Mice were sensitized intraperitoneally with OVA on days 1, 8, and 15, and administered saline, Dexamethasone (1.5 mg/kg), or FJE (50, 100, or 200 mg/kg) once a day for 16 days. Nasal symptoms, inflammatory cells, OVA-specific immunoglobulins, cytokine production, mast cell activation, and nasal histopathology were assessed. Administration of FJE down-regulated OVA-specific IgE and up-regulated OVA-specific IgG2a in serum. FJE reduced the production of T helper (Th) type 2 cytokines, and the Th1 cytokine levels were enhanced in nasal and bronchoalveolar lavage fluid. Moreover, FJE positively regulated allergic responses by reducing the accumulation of inflammatory cells, improving nasal and lung histopathological characteristics, and inhibiting inflammation-associated cytokines. FJE positively modulated the IL-33/TSLP/NF-B signaling pathway, which is involved in regulating inflammatory cells, immunoglobulin levels, and pro-inflammatory cytokines at the molecular level.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10420321PMC
http://dx.doi.org/10.3390/ijms241512514DOI Listing

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