JOURNAL OF CHROMATOGRAPHY B-ANALYTICAL TECHNOLOGIES IN THE BIOMEDICAL AND LIFE SCIENCES
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2023
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IF 3
Ping Huang,Bailu Duan,Deshun Li,Yanfen Duan,Zhenxiang Zhou,Lintao Han,Jingjing Li,Jiajia Wu,Yan Ye,Fengyun Zhang,Ziwen Guo,Qiong Wang,Fang Huang
Xixin-Ganjiang Herb Pair (XGHP), a classic combination treatment to warm the lungs and dissolve phlegm, is widely used in the treatment of various pulmonary diseases. Chronic obstructive pulmonary disease (COPD) refers to a group of chronic obstructive airway diseases that can seriously harm human health. However, the effective components, targets, and pathways that underlie XGHP in the treatment of COPD remain unclear. Therefore, this study initially identified the effective components of XGHP through the use of UPLC–MS/MS and pharmacologic methods of traditional Chinese medicine. Secondly, transcriptomic analysis of the lung tissues of rats revealed the pharmacodynamic transcripts of each group, and metabolomics analysis revealed the differential metabolites associated with XGHP treatment. Finally, molecular docking of effective components with transcriptome genes was performed and western blotting was performed in order to determine the expression of related proteins in rat lung tissue. Overall, 30 effective components of XGHP were identified, including L-asarinin, 6-gingerol, sesamin, kaempferol, and quercetin. Transcriptomic studies demonstrated that expression of 386 genes recovered after XGHP treatment, and that they were mainly enriched in the oxidative phosphorylation and AMPK signaling pathways. According to the metabolomics studies, expression of eight metabolites differed between the COPD and the XGHP groups. These metabolites were mainly involved the biosynthesis of unsaturated fatty acids. Finally, the transcriptomic and metabolomics data were integrated. FASN and SCD in AMPK signaling pathway were directly linked to certain metabolites, including linoleic acid, palmitic acid, and oleic acid. These results indicate that XGHP can inhibit pAMPK expression and negatively regulate FASN and SCD expression during treatment of COPD in order to enhance the biosynthesis of unsaturated fatty acids and maintain energy homeostasis.
研究领域:
药理学
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分子生物学
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中医药学
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慢性肺部疾病
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PubMed
高影响因子
CYTOTECHNOLOGY
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2026
·Vol. 78
·期 4
·156
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IF 2.2
Zhang Yougen,Gu Li,Zhang Xiaoyang,Ran Wei,Yan Yanfeng,Gu Hongwei
Pulmonary inflammation is a key feature of chronic obstructive pulmonary disease (COPD), contributing to disease progression and morbidity. However, the molecular mechanisms underlying therapeutic interventions remain to be fully elucidated. This study aimed to investigate the mechanisms of naringenin in modulating COPD-related pulmonary inflammation. Using an integrated approach combining network pharmacology, molecular docking, and in vitro/in vivo models, we systematically explored the effects of naringenin. Network pharmacology analysis identified NF-κB as a central target, which was validated through molecular docking and dynamics simulations showing stable binding between naringenin and NF-κB. In vitro, cigarette smoke extract-challenged lung epithelial cells treated with naringenin exhibited reduced cytotoxicity, downregulated TNF-α, phospho-NF-κB p65, and NLRP3 expression, inhibited Caspase-1 activation, and attenuated IL-1β maturation, and suppressed Gasdermin D cleavage. In vivo, naringenin-treated COPD mice displayed diminished pulmonary inflammatory cell infiltration, milder histopathological lung damage, decreased serum TNF-α/IL-1β levels, and inhibited activation of the NF-κB/NLRP3/Caspase-1 axis in lung tissue. Collectively, these findings reveal that naringenin alleviates COPD pulmonary inflammation and pyroptosis by targeting the NF-κB/NLRP3/Caspase-1 signaling cascade, providing mechanistic insights for traditional Chinese medicine-based COPD therapies. Graphical abstract
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PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
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2024
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IF 4.8
Sensen Li,Juan Cao,Zhongjie Yang,Shaoju Jin,Lei Yang,Hao Chen
Background Chronic obstructive pulmonary disease (COPD) is a chronic respiratory disease. Licorice and dried ginger decoction (LGD) is traditional Chinese medicine prescription with multiple effects. Glycyrrhetinic acid (GA) is the main bioactive components of LGD, which has been proven to have a relieving effect on various inflammatory diseases. Siglec-1 is a cell surface sialoadhesin and has been confirmed to be overexpressed in COPD and facilitate inflammatory reaction. This study is aimed to probe the interaction between LGD, GA, and siglec-1. Methods Cigarette smoke (CS) combined with lipopolysaccharide (LPS) treatment was utilized to construct a COPD rat model. Cigarette smoke extract (CSE) was utilized to induce alveolar macrophage NR8383 to construct a COPD cell model. HE staining was applied for measuring histopathological changes of COPD rats. Enzyme-linked immunosorbent assay (ELISA), reverse transcription real-time polymerase chain reaction (RT-qPCR), and western blot were applied for testing the concentrations and expressions of proinflammatory factors. High performance liquid chromatography-tandem mass spectrometry (HPLC-MS) analysis was utilized to determine the combination between siglec-1 and GA. JC-1 assay was utilized to evaluate mitochondrial function. Reactive oxygen species (ROS) production was tested by dichloro-dihydro-fluorescein diacetate (DCFH-DA) staining. Results LGD treatment notably alleviated lung injury and inflammatory response in COPD rats. In CSE-induced cells, LGD treatment suppressed the contents of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-8. Sialic-acid-binding Ig-like lectin 1 (Siglec-1) expression induced by CS was decreased after LGD treatment. Furthermore, we proved that GA could target siglec-1 to regulate the inflammatory response in COPD rats and cells . Additionally, GA could reduce ROS production and alleviate mitochondrial dysfunction to suppress COPD progression. Conclusion LGD inhibits inflammation and alleviates mitochondrial dysfunction in COPD by targeting siglec-1.
研究领域:
药理学
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呼吸病学
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中医
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分子生物学
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DOI
PubMed
高影响因子
TROPICAL JOURNAL OF PHARMACEUTICAL RESEARCH
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2022
·Vol. 21
·期 10
·2139-2146
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IF 0.523
Limei Du,Xinglan Huo,Ying Liu
Purpose: To study the influence of resveratrol on chronic obstruction in Aspergillus fumigatus infection-induced chronic lung disease (COPD) in rats, and the process involved.
Methods: Seventy-five Sprague Dawley SD) rats were assigned to blank control, COPD model, Aspergillus fumigatus-infected COPD model, low (100 mg/kg) and high-dose (200 mg/kg) resveratrol groups, with 15 rats in each group. Enzyme-linked immunosorbent assay (ELISA) was used to assay IL-6, IL-8 and TNF-α in bronchoalveolar lavage fluid (BALF), while lung protein concentrations of AMPK and PGC-1α were assayed by immunoblotting.
Results: In low- and high-dose resveratrol groups, inflammatory factor levels were significantly lower than the corresponding levels in COPD model and Aspergillus fumigatus-infected COPD model (p < 0.05), while lung tissue proteins of AMPK, PGC-1α, and AQP5 of the rats given high-dose resveratrol were significantly raised, relative to corresponding levels in rats given low-dose resveratrol (p < 0.05).
Conclusion: Resveratrol modulates expression levels of secretory factors and surface markers in alveolar macrophages in COPD model rats infected with Aspergillus fumigatus. Resveratrol exerts this effect through the regulation of AMPK/PGC-1α signaling pathway.
研究领域:
药理学
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免疫学
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呼吸医学
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高影响因子
International Journal of Chronic Obstructive Pulmonary Disease
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2022
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IF 2.893
Xiao Sun,Zhonghua Dong,Nan Li,Xiuli Feng,Yan Liu,Ang Li,Xiaosong Zhu,Chunyan Li,Zhongxi Zhao
Background Ophiocordyceps sinensis (C. sinensis) extracts have been found to have a therapeutic effect on patients with chronic obstructive pulmonary disease (COPD). Silent information regulator 1 (SIRT1) plays an important role in the regulation of inflammatory mediators and correlates with lung function and COPD exacerbations. The objective of this work was to explore the anti-inflammatory effect and preliminary pathways of nucleosides from cultured C. sinensis on RAW264.7 macrophages and COPD mice.Materials and methods The nucleosides were extracted from cultured C. sinensis powder and further purified by macroporous resin D101 and glucan G10 columns. Inflammation and oxidative stress models in RAW264.7 macrophages and in mice were established by injection of cigarette smoke extract (CSE). We then examined how the isolated nucleosides regulated the production of the associated inflammatory mediators in vitro and in vivo by enzyme-linked immunosorbent assay, reverse transcription polymerase chain reaction, and Western blot.Results The nucleosides inhibited inflammatory mediator expression of tumor necrosis factor-α, interleukin-6, interleukin-1β, and nitric oxide in both the CSE-stimulated RAW264.7 macrophages and mice. Moreover, the nucleosides elevated SIRT1 activation and suppressed nuclear factor-κB (NF-κB)/p65 activation in vitro and in vivo. Nucleoside treatment significantly decreased the levels of the inflammatory mediators in the bronchoalveolar lavage fluid (BALF) and serum of the CSE-induced mice. The nucleosides also altered the recruitment of inflammatory cells in BALF and improved characteristic features of the lungs in the CSE-induced mice.Conclusion These results show that the nucleosides suppressed COPD inflammation through the SIRT1–NF-κB/p65 pathway, suggesting that the nucleosides may be partly responsible for the therapeutic effects of cultured C. sinensis on COPD patients.
研究领域:
药理学
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免疫学
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呼吸病学
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分子生物学
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DOI
PubMed
高影响因子
Frontiers in Pharmacology
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2019
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IF 3.845
Ma Xiaoyao,Liu Aina,Liu Wenjuan,Wang Zhihua,Chang Nianwei,Li Suyun,Li Jiansheng,Hou Yuanyuan,Bai Gang
Chronic obstructive pulmonary disease (COPD) has been a major public health problem and is still a formidable challenge for clinicians. It is urgent to find new compounds for minimizing the risk of disease progression and exacerbation especially in the early phase of COPD. A traditional Chinese medicine (TCM) formula, Chuan Bei Pi Pa dropping pills (CBPP), was tested in this study to investigate its potential mechanisms in preventing the exacerbation of COPD. Phosphoproteomics analysis for a smog stimulated early stage COPD mice model was employed to detect the underlying molecular mechanisms of CBPP. In addition, protein–protein interaction (PPI) and bioinformatics analyses were included to analyze the key proteins and predict the key bioactive compounds. The results indicated that peiminine (PEI) target epidermal growth factor receptor (EGFR) prevented the exacerbation of COPD by inhibiting the EGFR signaling pathway, and ursolic acid (UA) can alleviate inflammation disorders via inhibition of CASP3 on mitogen-activated protein kinase (MAPK) signaling pathway. After in vivo and in vitro evaluations, we revealed that PEI from CBPP, as a lead compound, can improve lung function and alleviate pulmonary fibrosis by acting on the EGFR and MLC2 signaling pathways. Furthermore, the approach described here is an effective way to analyze and identify the bioactive ingredients from a mixture by functional proteomics analysis.
研究领域:
药理学
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呼吸病学
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蛋白质组学
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传统中药
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PubMed
高影响因子
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
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2021
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IF 3.575
Dandan Zheng,Jinglong Wang,Genju Li,Lulu An,Ying Qu,Qinxiu Zhang,Wenhui Ye,Xin Zhao,Zhongxi Zhao
Autophagy-impairment is involved in the pathological process of chronic obstructive pulmonary disease (COPD), and relates to inflammation and emphysema in lung injury. This study aimed to elucidate the protective effect of S -Allylmercapto- N -acetylcysteine (ASSNAC) against COPD via regulating the autophagy. Firstly, porcine pancreatic elastase (PPE)-induced COPD model in A549 cells was established, and ASSNAC was verified to alleviate the autophagy-impairment from the results of western blotting analysis of LC3BⅡ/Ⅰ and monodansylcadaverine (MDC) staining of autophagosome . Secondly, Balb/c mice were stimulated by PPE to induce the COPD model in vivo . The histological analysis of lung tissues presented that ASSNAC could alleviate the lung injury induced by PPE. Thirdly, the secretions of NO , TNF- α and IL-1 β in serum and BALF were reduced by ASSNAC compared with the PPE group. Finally, the mechanism of therapeutic effects of ASSNAC against COPD through regulating the autophagy-impairment was clarified. That is, ASSNAC inhibits the phosphorylation of PI3K/Akt/mTOR signaling pathways. In a word, this research provides a reference for ASSNAC to be an effective drug for pulmonary diseases.
研究领域:
药理学
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肺病学
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分子生物学
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细胞生物学
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PubMed
高影响因子
PHYTOCHEMICAL ANALYSIS
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2025
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IF 2.6
Peng Yang,Hu-Dong Lv,Jie Wu,Fang Long,Jing Zhou,Cheng-Ying Wu,Jin-Di Xu,Shan-Shan Zhou,Qing-Ling Xiao,Song-Lin Li,Hong Shen
Introduction The role of macromolecular components in traditional Chinese medicines (TCMs) decoction remains poorly understood, primarily because of their structural complexity and limited systemic bioavailability. In the modernization of TCMs' decoctions, macromolecular components are often removed as “poor bioavailable impurities” by ethanol precipitation that might attenuate the efficacy thereof. Purpose A novel strategy integrating LC–MS-based serum pharmacochemistry, network pharmacology, and pharmacodynamics was developed to reveal the role of macromolecular components in TCMs' decoction, using Qi-Huo-Yi-Fei decoction (QH) treating chronic obstructive pulmonary disease (COPD) as a case study. Materials and Methods QH was separated into macromolecular components (QH-M) and small molecular components (QH-S) by ethanol precipitation. The absorbed components of QH and QH-S in serum were qualitatively and semiquantitatively analyzed by UPLC-QTOF-MS/MS. The differences in targets and pathways of the absorbed components were predicted by network pharmacology analysis. The therapeutic effects on pulmonary function, histopathology, and inflammation of QH, QH-S, and QH-M were comparatively investigated on a COPD rat model. Result A total of 103 components were identified in QH and QH-S, whereas 86 and 72 were detectable in QH- or QH-S-treated serum, respectively. The highest levels of absorbed components appeared from 15 to 60 min for QH-S and at 15 min for QH. The concentrations of most absorbed components of QH were twofold higher than those of QH-S. Their protein–protein interaction (PPI), herb–component–target networks, and GO/KEGG enrichment pathways were quite different, mainly in inflammatory, immunity, and cell apoptosis processes. QH-M improved pulmonary function, histopathology, and inflammatory infiltration, mainly on FVC ( p < 0.05), thickness/external diameter ( p < 0.01), Wac/Pbm ( p < 0.01), TNF-α ( p < 0.01), and IL-17 ( p < 0.05). Meanwhile, QH was more effective than QH-S, mainly on FEV0.3/FVC, MAN, GC/CC, TNF-α, and IL-17. Conclusion QH-M was not only effective independently on COPD but also showed integrative effects with the coexisting QH-S in improving their absorption, thus strengthening the component–target interactions, and consequently contributing to the COPD therapeutic effects of QH. Therefore, it was confirmed that QH-M was essential for QH's COPD therapy and should not be removed during the modern preparation development.
研究领域:
药理学
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分析化学
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系统生物学
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中医药学
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呼吸医学
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产品关联
DOI
PubMed
高影响因子
Gut Microbes
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2024
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IF 12.2
Yiting Liu,Longjie Li,Jing Feng,Bing Wan,Qiang Tu,Wei Cai,Fa Jin,Guiying Tang,Lígia R. Rodrigues,Xiuwei Zhang,Jia Yin,Yunlei Zhang
Chronic obstructive pulmonary disease (COPD), a condition primarily linked to oxidative stress, poses significant health burdens worldwide. Recent evidence has shed light on the association between the dysbiosis of gut microbiota and COPD, and their metabolites have emerged as potential modulators of disease progression through the intricate gut-lung axis. Here, we demonstrate the efficacy of oral administration of the probiotic Pediococcus pentosaceus SMM914 (SMM914) in delaying the progression of COPD by attenuating pulmonary oxidative stress. Specially, SMM914 induces a notable shift in the gut microbiota toward a community structure characterized by an augmented abundance of probiotics producing short-chain fatty acids and antioxidant metabolisms. Concurrently, SMM914 synthesizes L-tryptophanamide, 5-hydroxy-L-tryptophan, and 3-sulfino-L-alanine, thereby enhancing the tryptophan-melatonin pathway and elevating 6-hydroxymelatonin and hypotaurine in the lung environment. This modulation amplifies the secretion of endogenous anti-inflammatory factors, diminishes macrophage polarization toward the M1 phenotype, and ultimately mitigates the oxidative stress in mice with COPD. The demonstrated efficacy of the probiotic intervention, specifically with SMM914, not only highlights the modulation of intestine microbiota but also emphasizes the consequential impact on the intricate interplay between the gastrointestinal system and respiratory health.
研究领域:
微生物学
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呼吸病学
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胃肠病学
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免疫学
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DOI
高影响因子
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