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Article ; Online: Mechanic study based on untargeted metabolomics of Pi-pa-run-fei-tang on pepper combined with ammonia induced chronic cough model mice.

Jie, Xiao-Lu / Tong, Zhe-Ren / Xu, Xin-Yue / Wu, Jia-Hui / Jiang, Xing-Liang / Tao, Yi / Feng, Pei-Shi / Yu, Jin / Lan, Ji-Ping / Wang, Ping

Journal of ethnopharmacology

2024 Volume 326, Page(s) 117905

Abstract: Ethnopharmacological relevance: Pi-pa-run-fei-tang (PPRFT), a traditional Chinese medicine formula ...

Abstract	Ethnopharmacological relevance: Pi-pa-run-fei-tang (PPRFT), a traditional Chinese medicine formula with long-standing history, demonstrated beneficial effect on chronic cough. However, the mechanism underlying efficacy unclear. In current research, we explored the impact and molecular mechanism of chronic cough mouse stimulating with capsaicin combined with ammonia. Aim of the study: To investigate the metabolic modulating effects, and potential mechanisms underlying the therapeutic effect of PPRFT in chronic cough. Materials and methods: Chronic cough mouse models were created by stimulating mice by capsaicin combined with ammonia. Number of coughs and cough latency within 2 min were recorded. With lung tissue and serum samples collected for histopathology, metabolomics, RT-qPCR, immunohistochemistry, and WB analysis. Lymphocytes were isolated and flow cytometric assays were conducted to evaluate the differentiation between Th17 and Treg cell among CD4 Results: Results indicated that PPRFT obviously reduced the number of coughs, prolonged cough latency, reduced inflammatory cell infiltration and lung tissues damage, and decreased the serum level of IL-6, IL-1β, TNF-α, and IL-17 while increasing IL-10 levels. Notably, PPRFT suppressed Th17 cell divergence and promoted Treg cell divergence. Furthermore, serum metabolomic assays showed that 46 metabolites differed significantly between group, with 35 pathways involved. Moreover, mRNA levels of IL-6, NF-κB, IL-17, RORγT, JAK2, STAT3, PI3K and AKT in lung tissues remarkably reduced and mRNA levels of IL-10 and FOXP3 were elevated after PPRFT pretreatment. Additionally, PPRFT treatments decreased the protein levels of IL-6, NF-κB, IL-17, RORγT, p-JAK2, p-STAT3, p-PI3K, and p-AKT and increased the protein levels of IL-10 and FOXP3, but no significantly effects to the levels on JAK2, STAT3, PI3K, and AKT in the lungs. Conclusion: Conclusively, our result suggested the effect with PPRFT on chronic cough may be mediated through IL-6/JAK2/STAT3 and PI3K/AKT/NF-κB pathway, which regulate the differentiation between Th17 and Treg cell. This beneficial effect of PPRFT in capsaicin and ammonia-stimulated chronic cough mice indicates its potential application in treating chronic cough.
MeSH term(s)	Mice ; Animals ; Interleukin-10/metabolism ; Cytokines/metabolism ; Interleukin-17/metabolism ; NF-kappa B/metabolism ; Nuclear Receptor Subfamily 1, Group F, Member 3/metabolism ; Ammonia/metabolism ; Interleukin-6/metabolism ; Chronic Cough ; Capsaicin/pharmacology ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; T-Lymphocytes, Regulatory ; Forkhead Transcription Factors/metabolism ; RNA, Messenger/metabolism ; Th17 Cells
Chemical Substances	Interleukin-10 (130068-27-8) ; Cytokines ; Interleukin-17 ; NF-kappa B ; Nuclear Receptor Subfamily 1, Group F, Member 3 ; Ammonia (7664-41-7) ; Interleukin-6 ; Capsaicin (S07O44R1ZM) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Forkhead Transcription Factors ; RNA, Messenger
Language	English
Publishing date	2024-02-15
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	134511-4
ISSN	1872-7573 ; 0378-8741
ISSN (online)	1872-7573
ISSN	0378-8741
DOI	10.1016/j.jep.2024.117905
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Zs.A 1494: Show issues

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Article ; Online: Bu-Fei Yi-Shen Granules Reduce Acute Exacerbations in Patients with GOLD 3-4 COPD: A Randomized Controlled Trial.

Yu, Xue-Qing / Di, Jia-Qi / Zhang, Wei / Wei, Geng-Shu / Ma, Zhan-Ping / Wu, Lei / Yu, Xue-Feng / Zhu, Hui-Zhi / Zhou, Miao / Feng, Cui-Ling / Feng, Ji-Hong / Fan, Ping / Li, Jian-Sheng / Yang, Jian-Ya

International journal of chronic obstructive pulmonary disease

2023 Volume 18, Page(s) 2439–2456

Abstract: ... of Bu-fei Yi-shen granules (BYGs) for COPD.: Patients and methods: We conducted a multicenter ...

Abstract	Purpose: Chronic obstructive pulmonary disease (COPD) is a disease characterized by frequent acute exacerbations (AEs), especially in severe and very severe cases. We aimed to evaluate the efficacy and safety of Bu-fei Yi-shen granules (BYGs) for COPD. Patients and methods: We conducted a multicenter, randomized, double-blinded, placebo-controlled trial of 348 COPD patients with GOLD 3-4 COPD. The patients were randomly assigned into experimental or control groups in a 1:1 ratio. Patients in the experimental group were prescribed BYG, while those in the control group were administered a placebo, orally, twice daily, with 5 days on and 2 days off per week for 52 weeks. The outcomes included AEs, pulmonary function, clinical signs and symptoms, dyspnea scores (mMRC), quality of life scores, and a 6-minute walk test (6MWT). Results: A total of 280 patients completed the trial, including 135 patients in the experimental group and 145 in the control group. Compared to the control group, significant differences were observed in frequencies of AEs (mean difference: -0.35; 95% CI: -0.61, -0.10; Conclusion: BYG, as compared to a placebo, could significantly reduce the frequencies of AEs and AE-related hospitalizations for GOLD 3-4 COPD patients. Clinical symptoms, treatment satisfaction, quality of life, and exercise capacity improved. There was no significant improvement in mortality and pulmonary function.
MeSH term(s)	Humans ; Pulmonary Disease, Chronic Obstructive/diagnosis ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Quality of Life ; Lung ; Dyspnea ; Walking
Language	English
Publishing date	2023-11-06
Publishing country	New Zealand
Document type	Randomized Controlled Trial ; Multicenter Study ; Case Reports ; Clinical Trial
ZDB-ID	2212419-6
ISSN	1178-2005 ; 1176-9106
ISSN (online)	1178-2005
ISSN	1176-9106
DOI	10.2147/COPD.S413754
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Article ; Online: Network Pharmacology and Molecular Docking Analysis on Molecular Targets and Mechanisms of Fei Jin Sheng Formula in the Treatment of Lung Cancer.

Zhang, Yun-Chao / Gao, Wen-Cang / Chen, Wei-Jian / Pang, De-Xiang / Mo, Da-Yu / Yang, Min

Current pharmaceutical design

2023 Volume 29, Issue 14, Page(s) 1121–1134

Abstract: Background: Fei Jin Sheng Formula (FJSF) is widely used in clinical treatment of lung cancer ...

Abstract	Background: Fei Jin Sheng Formula (FJSF) is widely used in clinical treatment of lung cancer. But the underlying active ingredients and mechanisms are unclear. Objective: To investigate the active components and functional mechanisms of FJSF in treating lung cancer using a network pharmacology approach and molecular docking combined with Results: FJSF contained 272 active ingredients and 52 potential targets for lung cancer. GO enrichment analysis is mainly related to cell migration and movement, lipid metabolism, and protein kinase activity. KEGG pathway enrichment analysis mainly involves PI3K-Akt, TNF, HIF-1, and other pathways. Molecular docking shows that the compound Xambioona, quercetin and methyl palmitate in FJSF has a strong binding ability with NTRK1, APC, and DVL2. Analysis of the data in UCSC to analyze the expression of DVL2 in lung cancer shows that DVL2 was overexpressed in lung adenocarcinoma tissues. Kaplan-Meier analysis shows that the higher DVL2 expression in lung cancer patients was associated with poorer overall survival and poorer survival in stage I patients. It was negatively correlated with the infiltration of various immune cells in the lung cancer microenvironment. Conclusion: FJSF may play a role in inhibiting the occurrence and development of lung cancer by downregulating the expression of DVL2 in A549 cells through its active ingredient Methyl Palmitate. These results provide scientific evidence for further investigations into the role of FJSF and Methyl Palmitate in the treatment of lung cancer.
MeSH term(s)	Humans ; Molecular Docking Simulation ; Network Pharmacology ; Phosphatidylinositol 3-Kinases ; Lung Neoplasms/drug therapy ; A549 Cells ; Drugs, Chinese Herbal/pharmacology ; Drugs, Chinese Herbal/therapeutic use ; Tumor Microenvironment
Chemical Substances	Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Drugs, Chinese Herbal
Language	English
Publishing date	2023-05-04
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1304236-1
ISSN	1873-4286 ; 1381-6128
ISSN (online)	1873-4286
ISSN	1381-6128
DOI	10.2174/1381612829666230503164755
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Article ; Online: Bu-Fei Yi-Shen Granules Reduce Acute Exacerbations in Patients with GOLD 3–4 COPD

Yu XQ / Di JQ / Zhang W / Wei GS / Ma ZP / Wu L / Yu XF / Zhu HZ / Zhou M / Feng CL / Feng JH / Fan P / Li JS / Yang JY

International Journal of COPD, Vol Volume 18, Pp 2439-

A Randomized Controlled Trial

2023 Volume 2456

Abstract: Xue-Qing Yu,1,2,* Jia-Qi Di,2,* Wei Zhang,3 Geng-Shu Wei,4 Zhan-Ping Ma,5 Lei Wu,6 Xue-Feng Yu,7 ...

Abstract	Xue-Qing Yu,1,2,* Jia-Qi Di,2,* Wei Zhang,3 Geng-Shu Wei,4 Zhan-Ping Ma,5 Lei Wu,6 Xue-Feng Yu,7 Hui-Zhi Zhu,8 Miao Zhou,9 Cui-Ling Feng,10 Ji-Hong Feng,11 Ping Fan,12 Jian-Sheng Li,1,2 Jian-Ya Yang1 1Department of Respiratory Disease, the First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, Henan Province, 450000, People’s Republic of China; 2Co-Construction Collaborative Innovation Center for Chinese Medicine and Respiratory Diseases by Henan & Education Ministry of P.R. China, Henan University of Chinese Medicine, Zhengzhou, Henan, 450046, People’s Republic of China; 3Department of Respiratory Disease, Shanghai Shuguang Hospital, Shanghai University of Chinese Medicine, Shanghai, 200000, People’s Republic of China; 4Department of Respiratory Disease, the Affiliated Hospital of Shaanxi University of Chinese Medicine, Xianyang, Shaanxi Province, 712000, People’s Republic of China; 5Department of Respiratory Disease, Shaanxi Province Hospital of Traditional Chinese Medicine, Xi’an, Shaanxi Province, 710000, People’s Republic of China; 6Department of Respiratory Disease, Hebei Province Hospital of Traditional Chinese Medicine, Shijiazhuang, Hebei, 050000, People’s Republic of China; 7Department of Respiratory Disease, the Second Affiliated Hospital of Liaoning University of Traditional Chinese Medicine, Shenyang, Liaoning Province, 110000, People’s Republic of China; 8Department of Respiratory Disease, the First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, Anhui Province, 230000, People’s Republic of China; 9Department of Respiratory Disease, the Third Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, Henan Province, 450000, People’s Republic of China; 10Department of Traditional Chinese Medicine, People’s Hospital Affiliated to Peking University, Beijing, 100000, People’s Republic of China; 11Department of Respiratory Disease, the Second Affiliated Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, 300000, People’s ...
Keywords	chronic obstructive pulmonary disease ; traditional chinese medicine ; efficacy ; safety ; rct ; Diseases of the respiratory system ; RC705-779
Language	English
Publishing date	2023-11-01T00:00:00Z
Publisher	Dove Medical Press
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Tiao-Bu-Fei-Shen Formula Improves Glucocorticoid Resistance of Chronic Obstructive Pulmonary Disease via Downregulating the PI3K-Akt Signaling Pathway and Promoting GR

Zhou, Pengcheng / Ma, Jianli / Yu, Wei / Chen, Keling / Zhang, Wensheng / Zhou, Jiang

Evidence-based complementary and alternative medicine : eCAM

2023 Volume 2023, Page(s) 4359616

Abstract: Objective: To predict and determine the mechanism through which Tiao-Bu-Fei-Shen (TBFS) formula ...

Abstract	Objective: To predict and determine the mechanism through which Tiao-Bu-Fei-Shen (TBFS) formula improves glucocorticoid resistance in chronic obstructive pulmonary disease (COPD), using network pharmacology, molecular docking technology, and Methods: The main active components and associated targets of TBFS were screened using the systems pharmacology database of traditional Chinese medicine database (TCMSP). The main COPD targets were retrieved from the Human Gene (GeneCards) and DrugBank databases. A protein-protein interaction (PPI) network was constructed using the protein interaction platform STRING and Cytoscape 3.6.1. Gene ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genome Pathway (KEGG) analyses were performed using the biological information annotation database Metascape. Molecular docking was performed using the AutoDock Vina software. THP-1 monocytes were treated with TBFS-containing serum and cigarette smoke extract (CSE) for 48 h, and cell proliferation in each group was determined using cell counting kit-8 (CCK-8). A COPD cell model was constructed by stimulating THP-1 monocytes with CSE for 12 h. A lentivirus vector for RNA interference of histone deacetylase 2 (HDAC2) gene was constructed and transfected into the THP-1 monocytes, and the transfection efficiency was verified using quantitative polymerase chain reaction (qPCR) and western blotting (WB). The expression of HDAC2 in each group of cells was detected using qPCR, and the expression of HDAC2, phosphoinositide-3 kinase (PI3K) p85 Results: A total of 344 TBFS active components, 249 related drug targets, 1,171 COPD target proteins, and 138 drug and disease intersection targets were obtained. Visual analysis of the PPI network map revealed that the core COPD targets of TBFS were AKT1, IL-6, TNF, TP53, and IL1- Conclusion: TBFS treatment improves glucocorticoid resistance observed in COPD through downregulation of the PI3K-Akt signaling pathway and promotion of GR
Language	English
Publishing date	2023-02-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	2171158-6
ISSN	1741-4288 ; 1741-427X
ISSN (online)	1741-4288
ISSN	1741-427X
DOI	10.1155/2023/4359616
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 5995: Show issues

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Article ; Online: Tiao-bu-fei-shen formula promotes downregulation of the caveolin 1-p38 mapk signaling pathway in COPD - Associated tracheobronchomalacia cell model.

Zhou, Pengcheng / Yu, Wei / Zhang, Chuantao / Chen, Keling / Tang, Wenjun / Li, Xuelian / Liu, Zijun / Xia, Qianming

Journal of ethnopharmacology

2022 Volume 293, Page(s) 115256

Abstract: Ethnopharmacological relevance: The Tiao-bu-fei-shen (TBFS) formula, extensively used ...

Abstract	Ethnopharmacological relevance: The Tiao-bu-fei-shen (TBFS) formula, extensively used in Traditional Chinese Medicine (TCM), can enhance therapeutic efficacy and reduce the frequency of acute exacerbations of lung-kidney Qi deficiency in patients with chronic obstructive pulmonary disease (COPD). According to both TCM theory and long-term observation of practice, TBFS has become an effective treatment for COPD-associated tracheobronchomalacia (TBM). Aim of the study: To investigate the mechanism of the TBFS formula in treating COPD-associated TBM based on caveolin 1-p38 MAPK signaling and apoptosis. Materials and methods: A rat COPD model was prepared by exposure to smoking combined with tracheal lipopolysaccharide injection. The trachea or bronchus chondrocytes from COPD rats were isolated, cultured, and treated with 10 ng/mL IL-1β for 24 h to develop a model of COPD-associated TBM. Normal rats were administered TBFS to prepare drug-containing serum, and CCK8 assays were used to screen the optimal drug-containing serum concentration and SB203580 dose. TBFS drug-containing serum and SB203580 were processed separately for the control, model, drug-containing serum, blocker, and drug-containing serum combined with blocker groups. Flow cytometry and CCK8 assays were used to detect apoptosis and proliferative activity. Toluidine blue staining and immunohistochemistry were used to analyze the chondrocyte proteoglycan and type II collagen content. Western blotting was used to detect the expression of caveolin 1, p-p38 MAPK, TNF-α, IL-1β, MMP-13, Bax, and Bcl-2 proteins. Quantitative PCR was used to detect the expression of caveolin 1, p38 MAPK, IL-1β, MMP-13, Bax, Bcl-2, and miR-140-5p. Results: The isolation and identification of bronchial chondrocytes from COPD rats revealed that 10 ng/mL IL-1β can produce a stable COPD-associated TBM model. Screened via the CCK8 method, fourth-generation bronchial chondrocytes were determined as the optimal cells, and 5 μM SB203580 and 5% low-dose drug-containing serum were the optimal intervention doses. The experimental chondrocytes of each group were treated separately for 48 h. Toluidine blue staining and immunohistochemical analysis revealed that TBFS drug-containing serum, SB203580, and TBFS drug-containing serum combined with SB203580 can effectively increase the proteoglycan and type II collagen content after chondrocyte degradation. Flow cytometry of cells treated with SB203580 and TBFS drug-containing serum combined with SB203580 revealed significantly reduced cell apoptosis and enhanced cell proliferation activity. Western blot and qPCR analyses revealed that the TBFS drug-containing serum, SB203580, and TBFS drug-containing serum combined with SB203580 effectively inhibit the expression of caveolin 1, p-p38 MAPK, MMP-13, IL-1β, TNF-α, and Bax proteins while promoting Bcl -2 protein expression. Treatment with TBFS drug-containing serum and SB203580 effectively inhibited the expression of MMP-13, p38 MAPK, caveolin 1, and Bax genes, and promoted the expression of Bcl-2 and miR-140-5p genes. Conclusions: A concentration of 10 ng/mL of IL-1β can generate a stable COPD-associated TBM cell model. TBFS can improve the proteoglycan and type II collagen content, increase cell activity, and reduce the amount of chondrocyte apoptosis. The role of TBFS may be related to mechanisms of inhibiting the expression of the key signaling molecules caveolin 1 and p-p38 MAPK in the caveolin 1-p38 MAPK signaling pathway, thereby reducing the expression of the downstream effector products MMP-13, IL-1β, and TNF-α, while inhibiting the expression of the apoptotic gene Bax and improving the expression of Bcl-2 and miR-140-5p genes.
MeSH term(s)	Animals ; Apoptosis ; Caveolin 1/genetics ; Chondrocytes ; Collagen Type II/metabolism ; Down-Regulation ; Humans ; Interleukin-1beta/metabolism ; Matrix Metalloproteinase 13/metabolism ; MicroRNAs/metabolism ; Proteoglycans/metabolism ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Pulmonary Disease, Chronic Obstructive/metabolism ; Rats ; Signal Transduction ; Tolonium Chloride/metabolism ; Tolonium Chloride/pharmacology ; Tracheobronchomalacia ; Tumor Necrosis Factor-alpha/metabolism ; bcl-2-Associated X Protein/metabolism ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	Caveolin 1 ; Collagen Type II ; Interleukin-1beta ; MicroRNAs ; Proteoglycans ; Proto-Oncogene Proteins c-bcl-2 ; Tumor Necrosis Factor-alpha ; bcl-2-Associated X Protein ; Tolonium Chloride (15XUH0X66N) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Matrix Metalloproteinase 13 (EC 3.4.24.-)
Language	English
Publishing date	2022-04-01
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	134511-4
ISSN	1872-7573 ; 0378-8741
ISSN (online)	1872-7573
ISSN	0378-8741
DOI	10.1016/j.jep.2022.115256
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Zs.A 1494: Show issues

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Article ; Online: Mechanism deconvolution of Qing Fei Pai Du decoction for treatment of Coronavirus Disease 2019 (COVID-19) by label-free integrative pharmacology assays.

Xu, Fangfang / Hou, Tao / Shen, Aijin / Jin, Hongli / Xiao, Yuansheng / Yu, Wenyi / Li, Xiaonong / Wang, Jixia / Liu, Yanfang / Liang, Xinmiao

Journal of ethnopharmacology

2021 Volume 280, Page(s) 114488

Abstract: ... known as Qing Fei Pai Du Decoction, has been demonstrated effective against Coronavirus Disease 2019 ...

Abstract	Ethnopharmacological relevance: Traditional Chinese medicine (TCM) has a long history in the prevention and treatment of pandemics. The TCM formula Lung Cleansing and Detoxifying Decoction (LCDD), also known as Qing Fei Pai Du Decoction, has been demonstrated effective against Coronavirus Disease 2019 (COVID-19). Aim of the study: This work aimed to elucidate the active ingredients, targets and pathway mechanism of LCDD related to suppression of inflammatory, immunity regulation and relaxation of airway smooth muscle for the treatment of COVID-19. Materials and methods: Mining chemical ingredients reported in LCDD, 144 compounds covering all herbs were selected and screened against inflammatory-, immunity- and respiratory-related GPCRs including GPR35, H1, CB2, B2, M3 and β2-adrenoceptor receptor using a label-free integrative pharmacology method. Further, all active compounds were detected using liquid chromatography-tandem mass spectrometry, and an herb-compound-target network based on potency and content of compounds was constructed to elucidate the multi-target and synergistic effect. Results: Thirteen compounds were identified as GPR35 agonists, including licochalcone B, isoliquiritigenin, etc. Licochalcone B, isoliquiritigenin and alisol A exhibited bradykinin receptor B2 antagonism activities. Atractyline and shogaol showed as a cannabinoid receptor CB2 agonist and a histamine receptor H1 antagonist, respectively. Tectorigenin and aristofone acted as muscarinic receptor M3 antagonists, while synephrine, ephedrine and pseudoephedrine were β2-adrenoceptor agonists. Pathway deconvolution assays suggested activation of GPR35 triggered PI3K, MEK, JNK pathways and EGFR transactivation, and the activation of β2-adrenoceptor mediated MEK and Ca Conclusions: This study elucidates the active ingredients, targets and pathways of LCDD. This is useful for elucidating multitarget synergistic action for its clinical therapeutic efficacy.
MeSH term(s)	Animals ; Biosensing Techniques/methods ; Cell Line, Tumor ; Chalcones/pharmacology ; Cricetulus ; Drugs, Chinese Herbal/analysis ; Drugs, Chinese Herbal/chemistry ; Drugs, Chinese Herbal/pharmacology ; Ephedrine/pharmacology ; HEK293 Cells ; Humans ; Immunity/drug effects ; Inflammation/metabolism ; Lung Diseases/metabolism ; Muscle, Smooth/drug effects ; Receptors, G-Protein-Coupled/metabolism ; Respiration/drug effects ; Signal Transduction/drug effects ; COVID-19 Drug Treatment
Chemical Substances	Chalcones ; Drugs, Chinese Herbal ; Receptors, G-Protein-Coupled ; qing fei pai du tang ; licochalcone B (G7383L14F6) ; Ephedrine (GN83C131XS)
Language	English
Publishing date	2021-08-03
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	134511-4
ISSN	1872-7573 ; 0378-8741
ISSN (online)	1872-7573
ISSN	0378-8741
DOI	10.1016/j.jep.2021.114488
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Article ; Online: Pi-Pa-Run-Fei-Tang alleviates lung injury by modulating IL-6/JAK2/STAT3/IL-17 and PI3K/AKT/NF-κB signaling pathway and balancing Th17 and Treg in murine model of OVA-induced asthma.

Jie, Xiao-Lu / Luo, Zi-Rui / Yu, Jin / Tong, Zhe-Ren / Li, Qiao-Qiao / Wu, Jia-Hui / Tao, Yi / Feng, Pei-Shi / Lan, Ji-Ping / Wang, Ping

Journal of ethnopharmacology

2023 Volume 317, Page(s) 116719

Abstract: Ethnopharmacological relevance: Pi-Pa-Run-Fei-Tang (PPRFT) is an empirical TCM prescription ...

Abstract	Ethnopharmacological relevance: Pi-Pa-Run-Fei-Tang (PPRFT) is an empirical TCM prescription for treating asthma. However, the underlying mechanisms of PPRFT in asthma treatment have yet to be elucidated. Recent advances have revealed that some natural components could ameliorate asthma injury by affecting host metabolism. Untargeted metabolomics can be used to better understand the biological mechanisms underlying asthma development and identify early biomarkers that can help advance treatment. Aim of the study: The aim of this study was to verification the efficacy of PPRFT in the treatment of asthma and to preliminarily explore its mechanism. Materials and methods: A mouse asthma model was built by OVA induction. Inflammatory cell in BALF was counted. The level of IL-6, IL-1β, and TNF-α in BALF were measured. The levels of IgE in the serum and EPO, NO, SOD, GSH-Px, and MDA in the lung tissue were measured. Furthermore, pathological damage to the lung tissues was detected to evaluate the protective effects of PPRFT. The serum metabolomic profiles of PPRFT in asthmatic mice were determined by GC-MS. The regulatory effects on mechanism pathways of PPRFT in asthmatic mice were explored via immunohistochemical staining and western blotting analysis. Results: PPRFT displayed lung-protective effects through decreasing oxidative stress, airway inflammation, and lung tissue damage in OVA-induced mice, which was demonstrated by decreasing inflammatory cell levels, IL-6, IL-1β, and TNF-α levels in BALF, and IgE levels in serum, decreasing EPO, NO, and MDA levels in lung tissue, elevating SOD and GSH-Px levels in lung tissue and lung histopathological changes. In addition, PPRFT could regulate the imbalance in Th17/Treg cell ratios, suppress RORγt, and increase the expression of IL-10 and Foxp3 in the lung. Moreover, PPRFT treatment led to decreased expression of IL-6, p-JAK2/Jak2, p-STAT3/STAT3, IL-17, NF-κB, p-AKT/AKT, and p-PI3K/PI3K. Serum metabolomics analysis revealed that 35 metabolites were significantly different among different groups. Pathway enrichment analysis indicated that 31 pathways were involved. Moreover, correlation analysis and metabolic pathway analysis identified three key metabolic pathways: galactose metabolism; tricarboxylic acid cycle; and glycine, serine, and threonine metabolism. Conclusion: This research indicated that PPRFT treatment not only attenuates the clinical symptoms of asthma but is also involved in regulating serum metabolism. The anti-asthmatic activity of PPRFT may be associated with the regulatory effects of IL-6/JAK2/STAT3/IL-17 and PI3K/AKT/NF-κB mechanistic pathways.
MeSH term(s)	Mice ; Animals ; NF-kappa B/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Ovalbumin/toxicity ; Interleukin-6/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Lung Injury/chemically induced ; Lung Injury/drug therapy ; Lung Injury/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Interleukin-17/metabolism ; T-Lymphocytes, Regulatory ; Disease Models, Animal ; Cytokines/metabolism ; Asthma/chemically induced ; Asthma/drug therapy ; Asthma/metabolism ; Signal Transduction ; Lung ; Immunoglobulin E ; Superoxide Dismutase/metabolism ; Mice, Inbred BALB C
Chemical Substances	NF-kappa B ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Ovalbumin (9006-59-1) ; Interleukin-6 ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Tumor Necrosis Factor-alpha ; Interleukin-17 ; Cytokines ; Immunoglobulin E (37341-29-0) ; Superoxide Dismutase (EC 1.15.1.1)
Language	English
Publishing date	2023-05-31
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	134511-4
ISSN	1872-7573 ; 0378-8741
ISSN (online)	1872-7573
ISSN	0378-8741
DOI	10.1016/j.jep.2023.116719
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Jian-Pi-Yi-Fei granule suppresses airway inflammation in mice induced by cigarette smoke condensate and lipopolysaccharide.

Tang, Cui-Ying / Tang, Si-Li / Huang, Kai-Feng / Xu, Jian / Yu, Hui / Lin, Lin

Indian journal of pharmacology

2019 Volume 51, Issue 4, Page(s) 263–268

Abstract: Introduction: As a chronic, progressive, and lethal pulmonary disease, chronic obstructive pulmonary disease (COPD) is lacking effective treatment. Chronic inflammatory processes, including inflammatory cytokines, play an important role with in its ... ...

Abstract	Introduction: As a chronic, progressive, and lethal pulmonary disease, chronic obstructive pulmonary disease (COPD) is lacking effective treatment. Chronic inflammatory processes, including inflammatory cytokines, play an important role with in its pathogenesis. Jianpiyifei (JPYF) granule is a traditional Chinese herbal formula historically used to strengthen the spleen and tonify the lung. JPYF is used clinically to treat stable COPD. However, whether the purported anti-inflammatory effect of JPYF in COPD involves regulation of key inflammatory cytokines is not clear. Materials and methods: The mice model of pulmonary inflammation was induced by lipopolysaccharide (LPS) and cigarette smoke condensate (CSC). The influence of JPYF on airway inflammation Results: The number of neutrophils and total cells in bronchoalveolar lavage fluid of the JPYF group were markedly lower than in the model group. The levels of interleukin (IL)-1 β and IL-6 were lower; tumor necrosis factor-alpha was downregulated, and IL-10 was higher in the JPYF group than the model group. In the JPYF group, histone deacetylase 2 (HDAC2) activity and protein expression were restored. Conclusion: The anti-inflammatory activity of JPYF involves the suppression of pro-inflammatory cytokines, enhanced IL-10 secretion, and the restoration of HDAC2 activity.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/therapeutic use ; Bronchoalveolar Lavage Fluid/cytology ; Bronchoalveolar Lavage Fluid/immunology ; Cytokines/immunology ; Female ; Histone Deacetylase 2/immunology ; Leukocyte Count ; Lipopolysaccharides ; Lung/drug effects ; Lung/immunology ; Lung/pathology ; Mice, Inbred BALB C ; Neutrophils/drug effects ; Neutrophils/immunology ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Pulmonary Disease, Chronic Obstructive/immunology ; Pulmonary Disease, Chronic Obstructive/pathology ; Smoke/adverse effects ; Tobacco Products
Chemical Substances	Anti-Inflammatory Agents ; Cytokines ; Lipopolysaccharides ; Smoke ; Hdac2 protein, mouse (EC 3.5.1.98) ; Histone Deacetylase 2 (EC 3.5.1.98)
Language	English
Publishing date	2019-10-01
Publishing country	India
Document type	Journal Article
ZDB-ID	605829-2
ISSN	1998-3751 ; 0253-7613
ISSN (online)	1998-3751
ISSN	0253-7613
DOI	10.4103/ijp.IJP_105_18
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 1983: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 311: Show issues

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Article: Tiao-bu-fei-shen formula promotes downregulation of the caveolin 1-p38 mapk signaling pathway in COPD - Associated tracheobronchomalacia cell model

Zhou, Pengcheng / Yu, Wei / Zhang, Chuantao / Chen, Keling / Tang, Wenjun / Li, Xuelian / Liu, Zijun / Xia, Qianming

Journal of ethnopharmacology. 2022 July 15, v. 293

2022

Abstract: The Tiao-bu-fei-shen (TBFS) formula, extensively used in Traditional Chinese Medicine (TCM ...

Abstract	The Tiao-bu-fei-shen (TBFS) formula, extensively used in Traditional Chinese Medicine (TCM), can enhance therapeutic efficacy and reduce the frequency of acute exacerbations of lung–kidney Qi deficiency in patients with chronic obstructive pulmonary disease (COPD). According to both TCM theory and long-term observation of practice, TBFS has become an effective treatment for COPD-associated tracheobronchomalacia (TBM). To investigate the mechanism of the TBFS formula in treating COPD-associated TBM based on caveolin 1–p38 MAPK signaling and apoptosis. A rat COPD model was prepared by exposure to smoking combined with tracheal lipopolysaccharide injection. The trachea or bronchus chondrocytes from COPD rats were isolated, cultured, and treated with 10 ng/mL IL-1β for 24 h to develop a model of COPD-associated TBM. Normal rats were administered TBFS to prepare drug-containing serum, and CCK8 assays were used to screen the optimal drug-containing serum concentration and SB203580 dose. TBFS drug-containing serum and SB203580 were processed separately for the control, model, drug-containing serum, blocker, and drug-containing serum combined with blocker groups. Flow cytometry and CCK8 assays were used to detect apoptosis and proliferative activity. Toluidine blue staining and immunohistochemistry were used to analyze the chondrocyte proteoglycan and type II collagen content. Western blotting was used to detect the expression of caveolin 1, p-p38 MAPK, TNF-α, IL-1β, MMP-13, Bax, and Bcl-2 proteins. Quantitative PCR was used to detect the expression of caveolin 1, p38 MAPK, IL-1β, MMP-13, Bax, Bcl-2, and miR-140–5p. The isolation and identification of bronchial chondrocytes from COPD rats revealed that 10 ng/mL IL-1β can produce a stable COPD-associated TBM model. Screened via the CCK8 method, fourth-generation bronchial chondrocytes were determined as the optimal cells, and 5 μM SB203580 and 5% low-dose drug-containing serum were the optimal intervention doses. The experimental chondrocytes of each group were treated separately for 48 h. Toluidine blue staining and immunohistochemical analysis revealed that TBFS drug-containing serum, SB203580, and TBFS drug-containing serum combined with SB203580 can effectively increase the proteoglycan and type II collagen content after chondrocyte degradation. Flow cytometry of cells treated with SB203580 and TBFS drug-containing serum combined with SB203580 revealed significantly reduced cell apoptosis and enhanced cell proliferation activity. Western blot and qPCR analyses revealed that the TBFS drug-containing serum, SB203580, and TBFS drug-containing serum combined with SB203580 effectively inhibit the expression of caveolin 1, p-p38 MAPK, MMP-13, IL-1β, TNF-α, and Bax proteins while promoting Bcl −2 protein expression. Treatment with TBFS drug-containing serum and SB203580 effectively inhibited the expression of MMP-13, p38 MAPK, caveolin 1, and Bax genes, and promoted the expression of Bcl-2 and miR-140–5p genes. A concentration of 10 ng/mL of IL-1β can generate a stable COPD-associated TBM cell model. TBFS can improve the proteoglycan and type II collagen content, increase cell activity, and reduce the amount of chondrocyte apoptosis. The role of TBFS may be related to mechanisms of inhibiting the expression of the key signaling molecules caveolin 1 and p-p38 MAPK in the caveolin 1–p38 MAPK signaling pathway, thereby reducing the expression of the downstream effector products MMP-13, IL-1β, and TNF-α, while inhibiting the expression of the apoptotic gene Bax and improving the expression of Bcl-2 and miR-140–5p genes.
Keywords	Oriental traditional medicine ; Western blotting ; apoptosis ; blood serum ; bronchi ; cell proliferation ; chondrocytes ; collagen ; flow cytometry ; genes ; immunohistochemistry ; lipopolysaccharides ; mitogen-activated protein kinase ; models ; protein synthesis ; proteoglycans ; quantitative polymerase chain reaction ; rats ; respiratory tract diseases ; therapeutics ; toluidine blue
Language	English
Dates of publication	2022-0715
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	134511-4
ISSN	1872-7573 ; 0378-8741
ISSN (online)	1872-7573
ISSN	0378-8741
DOI	10.1016/j.jep.2022.115256
Database	NAL-Catalogue (AGRICOLA)

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