Integrative Transcriptomic and Metabolomic Profiling Unravels Anti-Apoptotic and Anti-Inflammatory Properties of Qing-Jin-Hua-Tan Decoction in Chronic Obstructive Pulmonary Disease
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ABSTRACT:
PROVIDER: PRJNA924835 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23103162_1.fastq.gz | Fastqsanger.gz | |||
| SRR23103162_2.fastq.gz | Fastqsanger.gz | |||
| SRR23103163_1.fastq.gz | Fastqsanger.gz | |||
| SRR23103163_2.fastq.gz | Fastqsanger.gz | |||
| SRR23103164_1.fastq.gz | Fastqsanger.gz |
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Project description:Qing-Jin-Hua-Tan decoction (QJHTD) is a classic traditional Chinese medicine (TCM) prescription that has proven appropriate for the treatment of inflammatory lung diseases including chronic obstructive pulmonary disease (COPD), but its mechanism of action on COPD is still perplexing. We aim to explore the molecular machinery underpinning the curative effects of QJHTD on COPD. We confirmed in vitro anti-apoptotic and anti-inflammatory activities of QJHTD using the BEAS-2B and RAW264.7 cells challenged by cigarette smoke (CS) extract (CSE) and lipopolysaccharide (LPS) after chemical analysis of QJHTD. In vivo therapeutic activities of QJHTD were evaluated in the CS-LPS-exposed BALB/c mice. The phenotype data showed that anti-apoptotic and anti-inflammatory properties featured prominently in COPD treatment with QJHTD. Network pharmacology-based prediction followed by transcriptomic analysis of mouse lung tissue revealed that inhibiting such signaling pathways as IL-1β, IL-6, TNF, IκB-NF-κB, TLR, MAPK, and apoptosis contributed to the anti-COPD mechanism of QJHTD. Metabolome profiling unveiled the dominant role of dampening apoptosis and sphingolipid (SL) metabolism with choline (Ch) metabolism boosted in QJHTD modality for COPD. Integrative transcriptome-metabolome analysis unraveled the bridge between SL metabolism and apoptosis. In silico molecular docking revealed that acacetin as an active compound in QJHTD could bind with high affinities to the target proteins including MEK1, MEK2, ERK1, ERK2, Bcl2, NF-κB, and alCDase. These findings provide comprehensive insights into the molecular profile of QJHTD action against COPD and justify theoretical promise in a novel pharmacotherapy for the multifactorial disease.
2024-02-14 | GSE223102 | GEO
Project description:Qing-Jin-Hua-Tan-Decoction (QJHTD), a classic famous Chinese ancient prescription, has been used for treatment of pulmonary diseases since Ming Dynasty. A total of 22 prototype compounds of QJHTD absorbed into rat blood were chosen as candidates for the pharmacological network analysis and molecular docking. The targets from the intersection of compound target and ALI disease targets were used for GO and KEGG enrichment analyses. Molecular docking was adopted to further verify the interactions between 22 components and the top 20 targets with higher degree values in the component-target-pathway network. In vitro experiments were performed to verify the results of network pharmacology using SPR experiments, Western blot experiments, and the PMA-induced neutrophils to produce neutrophil extracellular trap (NET) model. The compound-target-pathway network includes 176 targets and 20 signaling pathways in which the degree of MAPK14, CDK2, EGFR, F2, SRC, and AKT1 is higher than that of other targets and which may be potential disease targets. The biological processes in QJHTD for ALI mainly included protein phosphorylation, response to wounding, response to bacterium, regulation of inflammatory response, and so on. KEGG enrichment analyses revealed multiple signaling pathways, including lipid and atherosclerosis, HIF-1 signaling pathway, renin-angiotensin system, and neutrophil extracellular trap formation. The molecular docking results showed that baicalin, oroxylin A-7-glucuronide, hispidulin-7-O-β-D-glucuronide, wogonoside, baicalein, wogonin, tianshic acid, and mangiferin can be combined with most of the targets, which might be the core components of QJHTD in treatment of ALI. Direct binding ability of baicalein, wogonin, and baicalin to thrombin protein was all micromolar, and their KD values were 11.92 μM, 1.303 μM, and 1.146 μM, respectively, revealed by SPR experiments, and QJHTD could inhibit Src phosphorylation in LPS-activated neutrophils by Western blot experiments. The experimental results of PMA-induced neutrophils to produce NETs indicated that QJHTD could inhibit the production of NETs. This study revealed the active compounds, effective targets, and potential pharmacological mechanisms of QJHTD acting on ALI.
| S-EPMC9304690 | biostudies-literature
Project description:The goal of this study is to compare the differently expressed genes in colon tissue of Control and DSS induced chronic colitis mouse model with or without Qing Hua Chang Yin (QHCY) treatment. The DSS induced chronic colitis mouse model were randomly divided into 3 groups: Model, Model + QHCY and Model + Mesalazine groups (n=6 for each group). Control mice (n=6) were set as control. Mice in Control and Model groups were intragastrically with double distilled water, while mice in Model + QHCY group was intragastrically with 1.6 g/kg/day of QHCY and mice in Model + Mesalazine group was intragastrically with 0.2 g/kg/d of Mesalazine. Then the colon tissues were used to identify differentially expressed genes among different groups.
2025-05-01 | GSE231888 | GEO
Project description:BackgroundQing-Jin-Hua-Tan decoction (QJHTD) is a classic traditional Chinese medicine (TCM) prescription that first appeared in the ancient book Yi-Xue-Tong-Zhi. QJHTD has shown effectiveness for treating chronic obstructive pulmonary disease (COPD), although its mechanisms of action are still perplexing. The molecular mechanisms underlying the curative effects of QJHTD on COPD is worth exploring.MethodsIn vitro antiapoptotic and antiinflammatory activities of QJHTD were evaluated using cell viability, proliferation, apoptosis rate, and expression of IL-1β and TNF-α in BEAS-2B and RAW264.7 cells challenged with cigarette smoke (CS) extract (CSE) and lipopolysaccharide (LPS). In vivo therapeutic activities of QJHTD were evaluated using respiratory parameters (peak inspiratory flow (PIFb) and peak expiratory flow (PEFb) values), histopathology (mean linear intercept, MLI), and proinflammatory cytokine (IL-1β and TNF-α) and cleaved caspase-3 (c-Casp3) levels in the lung tissue of CS-LPS-exposed BALB/c mice. Network pharmacology-based prediction, transcriptomic analysis, and metabolic profiling were employed to investigate the signaling molecules and metabolites pertinent to the anti-COPD action of QJHTD.ResultsIncreased cell viability and proliferation with decreased apoptosis rate and proinflammatory cytokine expression were noted after QJHTD intervention. QJHTD administration elevated PEFb and PIFb values, reduced MLI, and inhibited IL-1β, TNF-α, and c-Casp3 expression in vivo. Integrated network pharmacology-transcriptomics revealed that suppressing inflammatory signals (IL-1β, IL-6, TNF, IκB-NF-κB, TLR, and MAPK) and apoptosis contributed to the anti-COPD property of QJHTD. Metabolomic profiling unveiled prominent roles for the suppression of apoptosis and sphingolipid (SL) metabolism and the promotion of choline (Ch) metabolism in the anti-COPD effect of QJHTD. Integrative transcriptomics-metabolomics unraveled the correlation between SL metabolism and apoptosis. In silico molecular docking revealed that acacetin, as an active compound in QJHTD, could bind with high affinity to MEK1, MEK2, ERK1, ERK2, Bcl2, NF-κB, and alCDase target proteins.ConclusionThe therapeutic effect of QJHTD on COPD is dependent on regulating inflammatory signals and apoptosis-directed SL metabolism. These findings provide deeper insights into the molecular mechanism of action of QJHTD against COPD and justify its theoretical promise in novel pharmacotherapy for this multifactorial disease.
| S-EPMC10839876 | biostudies-literature
Project description:Protective effect of Qing Hua Chang Yin (QHCY) on ulcerative colitis
| PRJNA970066 | ENA
Project description:Qing Jin Hua Tan Tang (QJHTT) exerts therapeutic effects in patients with chronic obstructive pulmonary disease (COPD) by alleviating inflammation. However, the anti-inflammatory components of QJHTT have not yet been reported. Our study aimed to screen the active anti-inflammatory components of QJHTT using a multivariate statistical analysis approach for spectrum-effect relationships. Different polar fractions of QJHTT were prepared using ethanol, ethyl acetate, and n-butanol to analyze the phytochemical components. Phytochemical fingerprints were generated using ultrahigh-performance liquid chromatography. In total, 24 peaks were observed in ten batches of QJHTT extracts. The anti-inflammatory activity was evaluated using a xylene-induced ear-swelling mouse model. Additionally, the spectrum-effect relationship between the relative areas of the 24 peaks and pharmacological activity was investigated using multivariate statistical analysis. The potential anti-inflammatory ingredients obtained from the screening (multivariate statistical analysis) will be validated for their anti-inflammatory effects and mechanisms utilizing a lipopolysaccharide-induced macrophage inflammation model. QJHTT ethanol extract 1 exhibited good anti-inflammatory activity. Peaks 11, 12, 13, 14, and 16, which were closely correlated with anti-inflammatory activity, were identified as meranzin, baicalin, baicalein, chrysin-7-O-β-D-glucuronide, and wogonoside, respectively. The anti-inflammatory activities of meranzin, baicalin, baicalein, and wogonoside were verified in vitro. These four bioactive components significantly inhibited the secretion of inflammatory factors in the lipopolysaccharide-stimulated macrophage cell line. This research successfully screened the QJHTT anti-inflammatory active ingredient group. Meranzin, baicalin, baicalein, chrysin-7-O-β-D-glucuronide, and wogonoside were predicted to be the anti-inflammatory active ingredient groups of QJHTT.
| S-EPMC8380171 | biostudies-literature
Project description:BackgroundFei-Yan-Qing-Hua decoction (FYQHD) is derived from the well-known Ma Xing Shi Gan decoction, which was documented in Zhang Zhong Jing's "Treatise on Exogenous Febrile Disease" during the Han Dynasty. Although FYQHD has been used in the treatment of pneumonia and has demonstrated clinical efficacy for decades, the underlying mechanism by which FYQHD protects against influenza virus infection through modulation of gut flora remains unclear. Here, we examined the regulatory impacts of FYQHD on an influenza virus-infected mouse model and explored the mechanisms involved.MethodsAn infectious mouse model was created by intranasal instillation of influenza A virus (IAV). The effectiveness of FYQHD was assessed through various measures, including weight loss, lung wet/dry ratio, oxidative stress levels, viral load in lung tissues, and intestinal injuries. Changes in gut microbiota and SCFA production were also examined.ResultsThe results showed that FYQHD significantly reduced viral load, increased the production of type I interferon (IFN-I), and restored the integrity of the intestinal barrier following IAV challenge. Additionally, FYQHD significantly corrected the dysbiosis of gut microbiota induced by influenza virus infection, enhancing the abundance of SCFA-producing bacteria and acetate production. However, the depletion of gut microbiota significantly attenuated the protective effects of FYQHD against influenza virus infection. In vitro, the antiviral effect of acetate was demonstrated through the upregulation of concentrations of IFN-β.ConclusionFYQHD attenuates influenza virus-induced lung and intestinal injuries by boosting the host antiviral response through increasing the abundance of Lachnospiraceae_NK4A136 and Roseburia, along with elevated acetate levels. The study advances our understanding of the therapeutic mechanisms of FYQHD and provides a theoretical basis for the application of FYQHD in the treatment of influenza.
| S-EPMC11499185 | biostudies-literature
Project description:BackgroundJian Yun Qing Hua Decoction (JYQHD), a traditional Chinese medicine decoction, which has been applied in the treatment of gastric cancer (GC). We attempt to confirm the anti-gastric cancer effect of JYQHD and explore the mechanism of JYQHD.MethodsAcute toxicity test was used to understand the toxicity of JYQHD. We studied the expression and prognostic outcome of COL12A1 within GC tissues through the network databases. Using several web-based databases, we analyzed the major components and targets of JYQHD, as well as known therapeutic targets in gastric cancer. The Venn diagram was utilized to obtain the overlapped genes. Lentiviral vector, shRNAs and plasmids, were used to transfect GC cells. Cell counting kit-8 (CCK8), sphere formation, malondialdehyde (MDA), glutathione (GSH), reactive oxygen species (ROS), Fe2+, transmission electron microscopy (TEM), quantitative Real-Time Polymerase Chain Reaction (qRT-PCR), Western-Blot (WB), and immunohistochemical (IHC) assays were employed to investigate the role and mechanism of COL12A1 and JYQHD in GC.ResultsThe results showed that JYQHD was non-toxic and safe. JYQHD inhibited growth and sphere formation ability through inducing the ferroptosis of GC cells, and suppressed the GC cells induced subcutaneous xenograft tumor growth. COL12A1 was highly expressed in gastric cancer tissues, indicating poor prognosis. COL12A1 specifically enhanced GC cell progression and stemness via suppressing ferroptosis. JYQHD down-regulated COL12A1 in order to suppress the stemness of GC cells via inducing ferroptosis.ConclusionCOL12A1 inhibited ferroptosis and enhanced stemness in GC cells. JYQHD inhibited the development of GC cells by inhibiting cancer cell stemness via the ferroptosis pathway mediated by COL12A1.
| S-EPMC10496189 | biostudies-literature
Project description:ObjectiveThis study is dedicated to revealing the potential mechanism of Qin Run Hua Jie (QRHJ) decoction in Interstitial pneumonia (IP) treatment.MethodsThe TCMSP database predicted the chemical components and targets of QRHJ decoction, and the IP-related genes were from the Genecards database. Cytoscape software was used to establish the interaction network. R package clusterProfiler was utilized for Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. The molecular docking analysis of target proteins and the corresponding active pharmaceutical ingredients in the core position of the interaction network was conducted. Then, molecular dynamics (MD) simulations of a potential active substance and its key targets were performed. The binding efficiency of EGFR and luteolin, HIF1A and diosgenin was detected by cellular thermal shift assay (CETSA), and protein expression was measured by Western blot. CCK-8 was used to detect cell activity.ResultsA total of 153 active ingredients, 127 targets and 362 IP-related genes were obtained. KEGG enrichment analysis identified IP-related signaling pathways including HIF-1 signaling pathway and TNF signaling pathway. The two key components luteolin and diosgenin stably bound to the key targets EGFR and HIF1A. Cell experiments further showed that EGFR and luteolin, HIF1A and diosgenin bound to exert anti-fibrotic effects.ConclusionAs an active ingredient of QRHJ decoction, luteolin and diosgenin may exert therapeutic effect on IP through binding to the key target EGFR and HIF1A. This work initially revealed the key molecular mechanism of QRHJ decoction in IP treatment and offered theoretical evidence.
| S-EPMC10878319 | biostudies-literature