The current therapeutic interventions of chronic obstructive pulmonary disease offer only partial alleviation of symptoms, leaving the majority of patients with persistent and significant clinical manifestations. This investigation seeks to elucidate the underlying pharmacological mechanisms of Qing Fei Bao Yuan Decoction (QFBYD) employing a multidisciplinary approach that includes network pharmacology and molecular docking techniques. The QFBYD formulation were subjected to mass spectrometry analysis, while critical compounds and biological targets were subsequently identified through the TCMSP database. Disease- and drug-specific targets were collated from a plethora of databases, including Batman-TCM, Stitch, Swiss Target Prediction and GeneCards. GO and KEGG pathways were analyzed for the collected targets. A PPI network was constructed using STRING database to isolate core targets. Molecular docking was executed using Auto Dock Tools and PyMOL software, and an animal model of COPD was developed for experimental validation. Seven salient compounds and five core biological targets were ascertained through our analysis. Additionally, four compounds demonstrated high-affinity binding to the identified targets. Pathways involving bacterial endotoxin response, oxidative stress regulation, and endothelial cell migration were significantly enriched according to the KEGG database. Animal models substantiated that QFBYD ameliorated pathological hallmarks, enhanced respiratory functionality, mitigated overexpression of pro-inflammatory cytokines, augmented the antioxidant defense mechanism, and suppressed the hyperactivity of the five core targets. The efficacy of QFBYD in COPD treatment may be primarily attributed to its role in moderating inflammatory responses and rectifying oxidative imbalances.

Background: Obesity asthma is a unique asthma phenotype, which has the characteristics of aggravation of clinical symptoms, change of immune response, and resistance to standard treatment. Obese asthma, as a clinical refractory asthma type, urgently needs effective and side-effect-free treatment. Xuanbai Chengqi Decoction (XBCQD) is a traditional Chinese medicine prescription widely used in the treatment of lung diseases, including asthma in China. However, the efficacy and mechanism of obese asthma remain to be explored. Objectives: To elucidate the therapeutic effect of XBCQD on obese asthma and reveal its mechanism. Methods: Network pharmacology was used to predict the potential therapeutic targets and pathways of XBCQD in the treatment of obese asthma. We established a mouse model of obese asthma by feeding a high-fat diet combined with intraperitoneal injection of ovalbumin (OVA) to induce sensitization, and then intervened with intragastric administration of high, medium, and low doses of XBCQD. During the modeling period, lung function and body weight of mice were used to evaluate the preparation of the obese asthma model. H&E staining, RT-qPCR, ELISA, Western blot, and flow cytometry were used to quantify Th cell subsets, 16S rRNA sequencing was used to determine microbial composition, and GC/MS was used to detect the content of short-chain fatty acids in intestinal contents to explore the mechanism of Xuanbai Chengqi Decoction on obese asthma. Results: Network pharmacology showed that XBCQD may improve obese asthma by affecting core targets such as IL-6, TNF, and Caspase1, and through signaling pathways such as the IL-17 signaling pathway, AGE-RAGE signaling pathway, TNF signaling pathway, and Th17 cell differentiation. Experimental studies have found that XBCQD can alleviate the symptoms of obese asthma and lung inflammation, reduce serum IgE, reduce the expression of IL-6, IL-17, and IL-23 in serum, to reduce lung inflammation induced by obese asthma in mice; flow cytometry of spleen tissue showed that XBCQD reduced the proportion of Th17 cells and restored the proportion of Treg cells. Proteomics showed that XBCQD inhibited the expression of NLRP3, Caspase-1, and IL-1β by up-regulating the expression of GPR43, thereby inhibiting Th17-related protein RORγt and restoring Treg-related protein Foxp3, thereby regulating immune imbalance. At the same time, XBCQD restored the intestinal microbial species, and restored the beneficial bacteria such as Dubosiella , Akkermansia_muciniphila , Rikenella , which were reduced in obese asthmatic mice, and increased the content of acetic acid, propionic acid, and butyric acid in intestinal flora metabolites. Conclusion: XBCQD regulates Th17/Treg immune imbalance in obese asthma by improving intestinal microecology and regulating SCFAs/GPR43/NLRP3 pathway. These findings provide new pharmacological evidence for its clinical application in obese asthma.

Objectives: Tuberostemonine has several biological activity, the aim of study examined the impact of tuberostemonine on the proliferation of TGF-β1 induced cell model, and its ability to alleviate pulmonary fibrosis stimulated by bleomycin in mice. Methods: In vitro, we assessed the effect of tuberostemonine (350, 550 and 750 µM) on the proliferation of cells stimulated by TGF-β1 (10 μg/L), as well as on parameters such as α-SMA vitality, human fibronectin, collagen, and hydroxyproline levels in cells. In vivo, we analyzed inflammation, hydroxyproline, collagen activity and metabolomics in the lungs of mice. Additionally, a comprehensive investigation into the TGF-β/smad signaling pathway was undertaken, targeting lung tissue as well as HFL cells. Results: Within the confines of an in vitro setup, the tuberostemonine manifested a discerned IC50 of 1.9 mM. Furthermore, a significant reduction of over fifty percent was ascertained in the secretion levels of hydroxyproline, fibronectin, collagen type I, collagen type III and α-SMA. In vivo, tuberostemonine obviously improved the respiratory function percentage over 50% of animal model and decreased the hydroxyproline, lung inflammation and collagen deposition. A prominent decline in TGF-β/smad pathway functioning was identified within both the internal and external cellular contexts. Conclusions: Tuberostemonine is considered as a modulator to alleviate fibrosis and may become a new renovation for pulmonary fibrosis.

Depression is often associated with gastrointestinal issues, forming a self-sustaining cycle known as the emotion-gastrointestinal axis. Traditional Chinese Medicine (TCM) provides multi-component and multi-target therapies, though its mechanisms are not fully understood. This article reviews key studies on how TCM, including herbal formulas, single herbs, active ingredients, and acupuncture, influences the brain-gut axis in treating depression and gastrointestinal problems. This article reviews recent research on the pharmacological mechanisms of Chinese medicine, providing a basis for its targeted molecular therapy and future development. Additionally, it provides insights into enhanced treatment strategies for clinical patients and investigates the potential role of TCM in addressing depression and gastrointestinal-related health disorders.