ArticleInternational journal of chronic obstructive pulmonary disease2025
Effective-Component Compatibility of Bufei Yishen Formula (ECC-BYF) III Inhibits Mucus Hypersecretion by BEAS-2B Cells via miR-146a-5p-Mediated Regulation of the EGFR/MEK/ERK Pathway.
Article in International journal of chronic obstructive pulmonary disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Research progress on the mechanisms of mucus retention after mycoplasma pneumoniae infection.Frontiers in cellular and infection microbiology · 2026Review
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2 authors.
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Abstract
Purpose: To explore the role of the miR-146a-5p-mediated regulation of the EGFR/MEK/ERK pathway in the effect of effective-component compatibility of Bufei Yishen Formula III (ECC-BYF III) on ameliorating mucus hypersecretion by bronchial epithelial cells (BEAS-2B cells). Methods: BEAS-2B cells exposed to cigarette smoke extract (CSE) were used to establish a mucus hypersecretion model of BEAS-2B cells. The optimal intervention concentration of ECC-BYF III was screened by CCK-8, qRT-PCR and ELISA, the effects of ECC-BYF III on MUC5AC, MUC5B, IL-4, IL-8, TNF-α, IL-1α, miR-146a-5p and EGFR/MEK/ERK pathway expression were assessed. Furthermore, dual luciferase reporter gene was used to verify the relationship between miR-146a-5p and EGFR/MEK/ERK, and to observe the effect of down-regulating miR-146a-5p on ECC-BYF III ameliorating mucus hypersecretion and EGFR/MEK/ERK pathway. Results: ECC-BYF III reduced the expression of MUC5AC and MUC5B, decreased the mRNA expression of IL-1α, IL-8 and TNF-α, increased the mRNA expression of IL-4, and decreased the protein expression of TNF-α. Moreover, ECC-BYF III ameliorated CSE induced mucus hypersecretion in BEAS-2B cells through EGFR/MEK/ERK pathway. Finally, our results indicated that ECC-BYF III ameliorated the model by targeting miR-146a-5p and downregulating the EGFR/MEK/ERK pathway. Conclusion: ECC-BYF III can ameliorate CSE induced mucus hypersecretion by BEAS-2B cells and reduce the inflammatory response. The underlying mechanism may be related to the regulation of miR-146a-5p and the EGFR/MEK/ERK pathway. ECC-BYF III can inhibit activation of the EGFR/MEK/ERK pathway by upregulating the expression of miR-146a-5p, thereby ameliorating mucus hypersecretion by BEAS-2B cells.
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