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Ginsenoside Rd2 improves allergic asthma by inhibiting PTGS2 enzyme activity

ABSTRACT: This study aims to elucidate the molecular mechanisms underlying the therapeutic effects of mountain-grown ginseng in allergic asthma and to systematically identify and characterize bioactive monomeric compounds responsible for these effects. We found that total saponins from mountain-grown ginseng significantly alleviated asthmatic phenotypes. Further multi-omics analyses revealed that these effects may be mediated through modulation of the arachidonic acid metabolic pathway, particularly by regulating the enzymatic activity of the rate-limiting enzyme PTGS2, thereby suppressing the production of PGE2. Subsequent component identification using high-performance liquid chromatography, combined with computational modeling, identified ginsenoside Rd2 as a key bioactive compound. In vitro cellular experiments, together with site-directed mutagenesis of the predicted binding sites, further confirmed that Rd2 exerts inhibitory effects on PTGS2 enzymatic activity through specific molecular interactions. Collectively, these findings provide mechanistic insights into the anti-asthmatic effects of mountain-grown ginseng and highlight Rd2 as a promising bioactive compound targeting PTGS2, offering potential therapeutic value for allergic asthma.

INSTRUMENT(S): Liquid Chromatography MS - negative - reverse-phase, Liquid Chromatography MS - positive - reverse-phase

PROVIDER: MTBLS14268 | MetaboLights | 2026-04-13

REPOSITORIES: MetaboLights

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			Action	DRS
	a_MTBLS14268_LC-MS_negative_reverse-phase.txt	Txt
	a_MTBLS14268_LC-MS_positive_reverse-phase.txt	Txt
	i_Investigation.txt	Txt
	m_MTBLS14268_LC-MS_negative_reverse-phase_v2_maf.tsv	Tabular
	m_MTBLS14268_LC-MS_positive_reverse-phase_v2_maf.tsv	Tabular

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Project description:Background: In asthma, airway epithelium remodeling can already be detected during childhood, and epithelial cells are more susceptible to virus and oxidative stress. Their exact role in natural history and severity of children allergic respiratory disease remains however surprisingly unexplored. Aim: To analyze dysfunctions of epithelium in dust mite allergic respiratory disease (rhinitis ¬± asthma) in children. Methods: Expression profilings of nasal epithelial cells collected by brushing were performed on Affymetrix Hugene 1.0 ST arrays. All allergic patients were sensitized to dust mite. 19 patients had an isolated allergic rhinitis (AR). 14 patients had AR associated with asthma. Patients were compared to 12 controls, their severity and control being assessed according to NAEPP and ARIA criteria. Infections by respiratory viruses were excluded by real-time PCR measurements. Results: 61 probes were able to distinguish allergic rhinitis children from healthy controls. A majority of these probes was under the control of Th2 cytokines, as evidenced by parallel experiments performed on primary cultures of nasal epithelial cells. In uncontrolled asthmatic patients, we observed not only an enhanced expression of these Th2-responsive transcripts, but also a down-regulation of interferon-responsive genes. Conclusion: Our study identifies a Th2 driven epithelial phenotype common to all dust mite allergic children. Besides, it suggests that epithelium is involved in the severity of the disease. Expression profiles observed in uncontrolled asthmatic patients suggest that severity of asthma is linked at the same time to atopy and to impaired viral response. Nasal epithelium gene expression profiling of dust mite allergic children with isolated rhinitis, rhinitis associated with asthma and controls. 38 samples classified in 4 categories : 14 isolated rhinitis (R), 6 rhinitis with uncontrolled asthma (UA), 7 rhinitis with controlled asthma (CA) and 11 healthy subjects (C )

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Ginsenoside Rd2 improves allergic asthma by inhibiting PTGS2 enzyme activity

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