The bioflavonoid hispidulin effectively attenuates T helper type 2-driven allergic lung inflammation in the ovalbumin-induced allergic asthma mouse model

Respir Investig. 2024 Apr 23;62(4):558-565. doi: 10.1016/j.resinv.2024.04.012. Online ahead of print.

Abstract

Background: Allergic asthma affects nearly 300 million people worldwide and causes ahigh burden of disability and death. Effective treatments rely heavily on corticosteroids, which are associated with various complications. So, the alternative treatment is of significance. Hispidulin is a bioflavonoid found in herbs that were used in traditional medicine to treat inflammatory diseases, including asthma. This study aims to investigate the efficacy of hispidulin compound in the treatment of allergic lung inflammation using the mouse model of allergic asthma.

Methods: BALB/c mice were sensitized and challenged with chicken egg ovalbumin. Cells and cytokines from bronchoalveolar lavage (BAL) fluid were examined. Lung tissues were collected for histologic study. Mouse splenic CD4+ cells were cultured to observe the effect of hispidulin on T-helper 2 (Th2) cell differentiation in vitro.

Results: Hispidulin treatment could alleviate allergic airway inflammation as evidenced by a significant reduction in the inflammatory cell count and Th2 cytokines interleukin (IL)-4, IL-5, IL-13 in BAL fluid. Histologic examination of lung tissues revealed lower inflammatory cell infiltration to the bronchi and less airway goblet cell hyperplasia in the treatment group compared to the control group. At the cellular level, hispidulin (25, 50, and 100 μM) was found to directly suppress the differentiation and proliferation of Th2 cells and to suppress the production of Th2 cytokines, such as IL-4, IL-5, and IL-13, in vitro.

Conclusions: Hispidulin treatment was shown to effectively decrease type 2 lung inflammation in an ovalbumin-induced allergic asthma mouse model by directly suppressing Th2 cell differentiation and functions.

Keywords: Bioflavonoid; Hispidulin; Ovalbumin-induced allergic asthma mouse model; Th2 cytokines; Type 2 lung inflammation.