Journal of ethnopharmacology · 2025
Boehmeria nivea (L.) Gaud. ameliorates airway inflammation by inhibiting Th2 cell differentiation in allergic asthma.
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Lee Ba-Wool, Ha Ji-Hye, Yi Da-Hye, Kim Ju-Hong, Jeong Seong-Hun, Jeong Ju Hwan, Jung Kyungsook, Jeong Hyung Jae, Kwon Hyung-Jun, Park Ji-Young, Kim Woo Sik, Ryu Young-Bae, Kim Jong-Choon, Shin In-Sik, Lee In-Chul
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Boehmeria nivea (L.) Gaud. (BN) is a well-known traditional herbal medicine used to treat a wide range of conditions, including bleeding, fever, diarrhea, and wounds, as well as respiratory disorders such as cough and wheezing. However, its potential efficacy against allergic airway inflammation has yet to be systematically evaluated.
AIM OF THE STUDY: This study aimed to investigate the therapeutic potential of BN, particularly the ethyl acetate fraction (EA-BN), in modulating immune responses in allergic asthma.
MATERIAL AND METHODS: BALB/c mice were sensitized with ovalbumin (OVA) to induce allergic asthma and treated orally with BN fractions (100 mg/kg; EA-BN-L; 100 mg/kg and EA-BN-H; 200 mg/kg). Th2 cytokines (IL-4, IL-5, and IL-13) and inflammatory cell counts in bronchoalveolar lavage fluid (BALF) were measured. Bone marrow-derived dendritic cells (BMDCs) stimulated with lipopolysaccharide (LPS) and tumor necrosis factor (TNF)-α-stimulated NCI-H292 epithelial cells were used to assess in vitro potential effects. Flow cytometry and qPCR were used to evaluate cytokine levels and transcription factor expression.
RESULTS: This study demonstrated the significant efficacy of EA-BN in an OVA-induced allergic asthma model. EA-BN treatment markedly suppressed the expression of extracellular cytokines (IL-10, IL-12, and TNF-α), co-stimulatory molecules (CD80 and CD86), and MHC class I/II in both LPS-stimulated BMDCs and splenic DCs in OVA-induced asthmatic mice. In addition, EA-BN reduced GATA-3 expression in CD3+CD4+ T cells, suggesting inhibition of Th2 cell differentiation in splenic T cells from asthmatic mice. Histological analysis revealed that EA-BN attenuated mucus overproduction, and inflammatory cell infiltration in lung tissues, along with a concurrent decrease in Th2 cytokine levels and MUC5AC expression. Furthermore, EA-BN also inhibited Th2 cytokine expression in TNF-α-stimulated NCI-H292 cells.
CONCLUSION: EA-BN mediates its immunoregulatory effects by simultaneously suppressing dendritic cell activation and blocking Th2 cell differentiation, ultimately leading to the downregulation of Th2-driven inflammatory responses. These findings support EA-BN as a potential herbal therapeutic candidate for allergic asthma.
AIM OF THE STUDY: This study aimed to investigate the therapeutic potential of BN, particularly the ethyl acetate fraction (EA-BN), in modulating immune responses in allergic asthma.
MATERIAL AND METHODS: BALB/c mice were sensitized with ovalbumin (OVA) to induce allergic asthma and treated orally with BN fractions (100 mg/kg; EA-BN-L; 100 mg/kg and EA-BN-H; 200 mg/kg). Th2 cytokines (IL-4, IL-5, and IL-13) and inflammatory cell counts in bronchoalveolar lavage fluid (BALF) were measured. Bone marrow-derived dendritic cells (BMDCs) stimulated with lipopolysaccharide (LPS) and tumor necrosis factor (TNF)-α-stimulated NCI-H292 epithelial cells were used to assess in vitro potential effects. Flow cytometry and qPCR were used to evaluate cytokine levels and transcription factor expression.
RESULTS: This study demonstrated the significant efficacy of EA-BN in an OVA-induced allergic asthma model. EA-BN treatment markedly suppressed the expression of extracellular cytokines (IL-10, IL-12, and TNF-α), co-stimulatory molecules (CD80 and CD86), and MHC class I/II in both LPS-stimulated BMDCs and splenic DCs in OVA-induced asthmatic mice. In addition, EA-BN reduced GATA-3 expression in CD3+CD4+ T cells, suggesting inhibition of Th2 cell differentiation in splenic T cells from asthmatic mice. Histological analysis revealed that EA-BN attenuated mucus overproduction, and inflammatory cell infiltration in lung tissues, along with a concurrent decrease in Th2 cytokine levels and MUC5AC expression. Furthermore, EA-BN also inhibited Th2 cytokine expression in TNF-α-stimulated NCI-H292 cells.
CONCLUSION: EA-BN mediates its immunoregulatory effects by simultaneously suppressing dendritic cell activation and blocking Th2 cell differentiation, ultimately leading to the downregulation of Th2-driven inflammatory responses. These findings support EA-BN as a potential herbal therapeutic candidate for allergic asthma.