Abstract
Salidroside, an active component extracted from Rhodiola rosea, has been reported to inhibit allergic asthma. However, its mechanism has not been fully elucidated. Group 2 innate lymphoid cells (ILC2s) accumulate in the lung and cooperate with other cells to drive type 2 inflammation stimulated by inhaled allergens. The study aims to explore the suppressive effect of salidroside on ILC2s and IL-33/IL-33R (ST2) axis in allergic airway inflammation. The ovalbumin (OVA)-sensitized/challenged mice were established. Airway eosinophil recruitment, increased total IgE in the serum and type 2 cytokines IL-4, IL-5, and IL-13 in the bronchoalveolar lavage fluids and lung tissues were identified in the OVA-induced mice model, all of which were inhibited by pretreatment with different doses of salidroside. Moreover, salidroside suppressed lung total ILC2 and ST2-expressing ILC2 accumulation, lung IL-33 and ST2 expressions in mice. In vitro, OVA could induce IL-33 expression in BEAS-2B cells, which was also effectively inhibited by salidroside. This study firstly reveals salidroside as a potential therapeutic drug for allergic asthma by inhibiting ILC2-mediated airway inflammation via targeting IL-33/ST2 axis.
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