ArticleJournal of inflammation research2026
Deacetyl Ophiopojaponin A ameliorates Asthma by Inhibiting L-Type Calcium Channel Cav2.3 to Reduce Calcium Load in Airway Epithelial Cells.
Article in Journal of inflammation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Purpose: The in-house preparation Qingre Runzao formula (QRRZF) has been used for decades in our hospital to treat asthma with good efficacy, but its underlying mechanisms and key components remain unclear. This study aims to elucidate the potential mechanisms and key components by which the QRRZF ameliorates asthma. Methods: UPLC-MS/MS was employed to identify the components of the QRRZF; therapeutic targets were predicted with SwissTargetPrediction and Super-Pred. Asthma transcriptomic data were obtained from GEO and differentially expressed genes were identified (GSE43696 and GSE147878). Venn analysis yielded potential targets of the QRRZF against asthma. GO and KEGG enrichment analyses with Metascape identified key pathways; the pathway-associated proteins served as receptors for molecular docking to rank drug-receptor affinities, thereby identifying key anti-asthma components. CETSA was performed on 16HBE cells cultured in vitro to verify docking results. CCK-8 and ELISA assessed the anti-asthma effects of the key components in vitro, and an HDM-induced asthma mouse model evaluated its efficacy in vivo. Results: A total of 21 components and 827 predicted targets were obtained; 1250 asthma-related targets were extracted from GEO, yielding 76 potential therapeutic targets. Enrichment analysis suggested calcium signaling pathway as the main pathway; molecular docking showed Deacetyl Ophiopojaponin A (DOA) bound most tightly to Cav2.3, confirmed by CETSA. In vitro experiments demonstrated that DOA protected 16HBE cells from damage induced by house dust mites, reducing the levels of inflammatory cytokines and alleviating airway inflammation, such IL-6, IL-13, and TNF-α. In vivo experiments showed that DOA reduced inflammatory cell infiltration and airway inflammation in the lung bronchioles, protecting the epithelial barrier and demonstrating significant therapeutic efficacy. These results indicate that DOA exerts potent anti-asthma effects by inhibiting the Cav2.3 calcium channel. Conclusion: This study reveals that calcium signaling pathway is the principal mechanism by which QRRZF improves asthma, and DOA is the key therapeutic component, which alleviates asthma-induced airway inflammation by inhibiting Cav2.3 expression and reducing calcium load in airway epithelial cells.
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