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Metabolic abnormalities caused by the accumulation of human, environmental, genetic and lifestyle variables can be found in diabetes mellitus (DM). An increase in blood glucose carried on by a reduction in insulin production can also result in DM. Insulin resistance often occurs as a result of obesity and a lack of physical activity and aging. Telang flower extract (Clitoria ternatea L.) is reported to have several qualities such as being able to treat DM, chronic bronchitis, goiter, mucosal disorders and leprosy. This study's objective was to elucidate anti-dibetic effect of C. ternatea extract (CTE) in rats with diabetic complications related to dyslipidemia. Rats suffering from diabetes will be examined after being given oral doses of Simvastatin 0.9 mg/kg BW, Glibenclamide 0.45 mg/kg BW, and 200, 400, and 800 mg/kg BW CTE, model induced by streptozotocin. The expression of the insulin gene (INS-1) was investigated by qRTPCR, Tumor Necrosis Factor-α (TNF-α), and Interleukin-1β (IL-1β) pancreatic DM rats model using the Immunohistochemistry (IHC) test. Both descriptive and quantitative data were acquired for the data. After utilizing ANOVA to evaluate quantitative data, the Tukey post hoc test was used to analyze the data, the expression of TNF-α and IL-1β was found to decrease while INS-1 expression increased in response to CTE. This effect was attributed to the modulation of TNF-α, IL-1β, and INS-1 expression. These findings suggest that CTE possesses antidiabetic properties. [ABSTRACT FROM AUTHOR]

Excessive water consumption is an extremely rare and potential asthma risk factor with very few cases reported in the literature. Common triggers of asthma include genetic factors, smoking, allergens, and viral respiratory infections. The adult patient with asthma reportedly drank too much water and was unable to get relief from his asthma while hospitalized. The patient's asthma was better controlled with the use of diuretics and control of the patient's fluid intake and output. This case explores asthma induced by excessive drinking of water. [ABSTRACT FROM AUTHOR]

Background: The association between obesity and respiratory diseases has been confirmed. However, few studies have reported the relationship between obesity and the risk and mortality of chronic inflammatory airway disease (CIAD). The aim of this study was to reveal the association between obesity and the risk of CIAD, and mortality in patients with CIAD. Methods: The study was conducted using data from the National Health and Nutrition Examination Survey (NHANES) 2013 to 2018 among adults aged 20 years and above. All participants were grouped according to body mass index (BMI) and waist circumference (WC) levels to study the relationship between obesity and CIAD. Multivariate logistic regression analysis was utilized to examine the connection between CIAD and obesity in a cross-sectional study. The association between obesity and all-cause mortality in individuals with CIAD was examined using multiple cox regression models and smooth curve fitting in a prospective cohort study. Results: When stratified based on BMI in comparison to the normal weight group, the ORs with 95%CIs of CIAD for underweight and obesity were 1.39 (1.01–1.93) and 1.42 (1.27–1.58), respectively. The OR with 95%CI of CIAD for obesity was 1.20 (1.09–1.31) when stratified according to WC. Additionally, underweight was associated with a higher mortality (HR = 2.44, 95% CI = 1.31–4.55), whereas overweight (HR = 0.58,95% CI = 0.39–0.87) and obesity (HR = 0.59,95% CI = 0.4–0.87) were associated with a lower mortality (P for trend < 0.05). There was a non-linear association between BMI and all-cause mortality (P for non-linear = 0.001). An analysis of a segmentation regression model between BMI and all-cause mortality revealed a BMI turning point value of 32.4 kg/m2. The mortality of CIAD patients was lowest when BMI was 32.4 kg/m2. When BMI ≤ 32.4 kg/m2, BMI was inversely associated with all-cause mortality in patients with CIAD (HR: 0.92, 95%CI:0.88–0.97). However, when BMI > 32.4 kg/m2, there was no association between BMI and all-cause mortality (HR:1.02, 95%CI:0.97–1.06). Conclusion: Compared to normal weight, underweight and obesity were associated with the increased risk of CIAD. Underweight was associated with increased all-cause mortality, while overweight was associated with reduced all-cause mortality. There was a non-linear association between BMI and all-cause mortality in patients with CIAD. The all-cause mortality was lowest when BMI was 32.4 kg/m2. [ABSTRACT FROM AUTHOR]

Background: Invasive fungal disease (IFD) is a frequent complication in pediatric lung transplant recipients, occurring in up to 12% of patients in the first year. Risk factors for infection include impaired lung defenses and intense immunosuppressive regimens. While most IFD occurs from Aspergillus, other fungal conidia are continuously inhaled, and infections with fungi on a spectrum of human pathogenicity can occur. Case Report: We report a case of a 17‐year‐old lung transplant recipient in whom Irpex lacteus and Rhodotorula species were identified during surveillance bronchoscopy. She was asymptomatic and deemed to be colonized by Irpex lacteus and Rhodotorula species following transplant. 2 years after transplantation, she developed a fever, respiratory symptoms, abnormal lung imaging, and histological evidence of acute and chronic bronchitis on transbronchial biopsy. After developing symptoms concerning for a pulmonary infection and graft dysfunction, she was treated for a presumed IFD. Unfortunately, further diagnostic testing could not be performed at this time given her tenuous clinical status. Despite the initiation of antifungal therapy, her graft function continued to decline resulting in a second lung transplantation. Conclusions: This case raises the concern for IFD in lung transplant recipients from Irpex species. Further investigation is needed to understand the pathogenicity of this organism, reduce the incidence and mortality of IFD in lung transplant recipients, and refine the approach to diagnosis and manage the colonization and isolation of rare, atypical fungal pathogens in immunocompromised hosts. [ABSTRACT FROM AUTHOR]

The complex nature of chronic bronchitis (CB) and changing definitions have contributed to challenges in understanding its aetiology and burden. In children, CB is characterised by persistent airway inflammation often linked to bacterial infections and is therefore termed "protracted bacterial bronchitis" (PBB). Longitudinal studies suggest that CB in childhood persists into adulthood in a subgroup. It can also be associated with future chronic respiratory diseases including asthma, bronchiectasis, and chronic obstructive pulmonary disease (COPD). Adult CB is traditionally associated with smoking, occupational exposures, and lower socioeconomic status. The interplay between risk factors, childhood CB, adult CB, and other chronic respiratory diseases is intricate, requiring comprehensive longitudinal studies for a clearer understanding of the natural history of CB across the lifespan. Such longitudinal studies have been scarce to date given the logistic challenges of maintaining them over time. In this review, we summarise current evidence on the evolution of the definitions, pathophysiology, risk factors, and consequences of childhood and adulthood chronic bronchitis. [ABSTRACT FROM AUTHOR]

Objective: To explore the effects of paeoniflorin on Th17, Treg cell subsets and lung function in rats with chronic bronchitis （CB）, so as to enrich its pharmacological effects. Methods: CB model was established by compound induction in SD rats, and SD rats were randomly divided into CB group （normal saline）, low-dose paeoniflorin group （50 mg/kg）, medium-dose paeoniflorin group（ 100 mg/kg）, high-dose paeoniflorin group（ 200 mg/kg） and Helao group（ positive control, Helao oral liquid）, with 10 rats in each group; another 10 rats in the control group （normal saline） were given 2 ml/100 g corresponding drugs by gavage after modeling. After administration, the general conditions of rats were observed and the lung function and blood gas were analyzed; the morphology of lung tissue was observed by HE staining; the lung CD4+T, CD8+T, Th17（ CD4+IL-17+T） and Treg（ CD4+CD25+Foxp3+T） cells were detected by flow cytometry; the levels of IL-10, IL-22 and IL-17 in the lung were detected by ELISA. Results: In CB group, the activity of rats were slow, the color of hair were dim, the body were curled up, accompanied with cough and moist nasal cavity, the above symptoms and injuries were alleviated in different degrees in paeoniflorin groups and Helao group, and the high dose group was the least. Compared with control group, the airway resistance, arterial partial pressure of carbon dioxide （PaCO2）, IL-17, IL-22 levels, CD4+T, CD8+T, Th17 cells, Th17/Treg, CD4+T/CD8+T were higher in CB group, arterial partial pressure of oxygen （PaO2）, IL-10 and Treg cells were lower （all P<0.05）; compared with CB group, the airway resistance, PaCO2, IL-17, IL-22 levels, CD4+T, CD8+T, Th17 cells, Th17/Treg, CD4+T/CD8+T in low-, medium- and high-dose paeoniflorin groups decreased in turn, PaO2, IL-10 and Treg cells increased in turn （all P<0.05）; there was no significant difference in airway resistance and the other above indexes between the medium-dose paeoniflorin group and Helao group （P>0.05）. Conclusion: Paeoniflorin can regulate the activation of T lymphocytes, reduce the differentiation of Th17 cells, increase the differentiation of Treg cells, and reduce the inflammatory level and lung injury in CB rats. [ABSTRACT FROM AUTHOR]

The study aimed to assess associations between chronic diseases and incident and persistent depressive symptoms (DSs) in a cohort study of ageing adults in South Africa. Participants in the baseline survey (in 2014/2015) were 5,059 persons (≥40 years) and at follow-up 4,176 (in 2018/2019). DSs were measured with the Center for Epidemiological Studies Depression scale. Logistic regression was used to estimate the associations between chronic conditions and incident and persistent DS. The prevalence of DS at baseline was 15.5%, incident DS (without DS and/or PTSD at baseline) was 25.1% and persistent DS (DS at both baseline and follow-up) was 4.8%. In unadjusted logistic regression analysis, diabetes had higher odds of incident DS. Participants with baseline heart attack/stroke/angina, dyslipidemia, tuberculosis, chronic bronchitis, kidney disease and three or more chronic conditions had a higher probability of persistent DS. In conclusion, of the eight chronic conditions evaluated, only diabetes (in unadjusted analysis) was associated with incident DS, and five chronic conditions (heart attack/stroke/angina, dyslipidaemia, tuberculosis, chronic bronchitis and kidney disease) and three or more chronic conditions were associated with persistent DS. [ABSTRACT FROM AUTHOR]

Background: Cameroon is a tuberculosis (TB) burden country with a 12% positivity among TB presumptive cases. Of the presumptive cases with a negative TB test, some are infected with Non-tuberculous Mycobacteria (NTM). However, the diagnosis of NTM infections remains difficult due to the lack of tools in many laboratories, particularly in resource limited laboratories and remote setting. The present study was undertaken to determine NTM profile and associated comorbidities among TB presumptive people. Methods: A retrospective study was conducted from December 2018 to December 2019 in the Tuberculosis-National Reference Laboratory (TB-NRL) for Bacteriological analysis of samples and Jamot Hospital of Yaounde (JHY) for clinical evaluation of confirmed NTM patients. We included in this study data of 5267 TB presumptive people previously diagnosed using three consecutive samples and having culture and SD Bioline results with or without Microscopy and reverse hybridization-based Line Probe Assay(LPA) results. The data on co-morbidities or history of people infected with NTM were then collected from the three participants with available clinical data. Results: We collected data of 5267 presumptive TB people. Among them, 3436 (65.24%), have a positive culture with 3200 (60.75%) isolates belong to Mycobacterium tuberculosis Complex (MBTC) and 236 (4.48%) to NTM. Our results showed that, 123 (52.11%) NTM were isolated from people with negative microscopy and 113 (47.88%) from people with positive microscopy. Among the 236 NTM, 108 (45.8%) isolates were identified using LPA. M. fortuitum was the most represented species (32.41%) followed by M. intracellulare (19.44%). Sputum had the highest proportion of NTM (56%), followed by bronchial aspirations (31%). The extra-pulmonary samples presented lower proportions of isolates compared to pulmonary samples. Some patients affected with NTM presented comorbidities as HIV infection, Pulmonary tuberculosis, Type 2 diabetes, Chronic bronchitis and Alveolar pneumonia. Conclusions: Our study showed the presence of NTM strains among presumptive TB people with a predominance of M. fortuitum and M. intracellulare. It is important to implement a surveillance system of NTM in TB burden country and also to develop a point-of-care test for NTM identification in limited-resource settings. [ABSTRACT FROM AUTHOR]

Simple Summary: Lung cancer is one of the deadliest cancers worldwide, and the prognosis is poor. The disease is potentially curable if detected at an early stage, but currently, the only widely implemented screening tool is low-dose computed tomography. Biomarkers such as methylated tumor DNA may be used for the early detection of lung cancer, and sputum is an appealing, non-invasive sample type. With this systematic review and meta-analysis, we aimed to identify all studies evaluating the quantitative methylation of tumor DNA in sputum samples for lung cancer detection. A systematic overview of all the available evidence may highlight areas of improvement as well as certain high-performing genes to prioritize in future studies. Lung cancer is the leading cause of cancer-related mortality worldwide. Early diagnosis is pivotal for the prognosis. There is a notable overlap between lung cancer and chronic bronchitis, and the potential use of methylated tumor DNA in sputum as a biomarker for lung cancer detection is appealing. This systematic review and meta-analysis followed the PRISMA 2020 statement. A comprehensive search was conducted in Embase, Medline, Web of Science, and the Cochrane Library, using these search strings: Lung cancer, sputum, and methylated tumor DNA. A total of 15 studies met the eligibility criteria. Studies predominantly utilized a case–control design, with sensitivity ranging from 10 to 93% and specificity from 8 to 100%. A meta-analysis of all genes across studies resulted in a summary sensitivity of 54.3% (95% CI 49.4–59.2%) and specificity of 79.7% (95% CI 75.0–83.7%). Notably, two less explored genes (TAC1, SOX17) demonstrated sensitivity levels surpassing 85%. The study's findings highlight substantial variations in the sensitivity and specificity of methylated tumor DNA in sputum for lung cancer detection. Challenges in reproducibility could stem from differences in tumor site, sample acquisition, extraction methods, and methylation measurement techniques. This meta-analysis provides a foundation for prioritizing high-performing genes, calling for a standardization and refinement of methodologies before potential application in clinical trials. [ABSTRACT FROM AUTHOR]

Ground-level ozone ranks sixth among common air pollutants. It worsens lung diseases like asthma, emphysema, and chronic bronchitis. Despite recent attention from researchers, the link between exhaled breath and ozone-induced injury remains poorly understood. This study aimed to identify novel exhaled biomarkers in ozone-exposed mice using ultra-sensitive photoinduced associative ionization time-of-flight mass spectrometry and machine learning. Distinct ion peaks for acetonitrile (m/z 42, 60, and 78), butyronitrile (m/z 70, 88, and 106), and hydrogen sulfide (m/z 35) were detected. Integration of tissue characteristics, oxidative stress-related mRNA expression, and exhaled breath condensate free-radical analysis enabled a comprehensive exploration of the relationship between ozone-induced biological responses and potential biomarkers. Under similar exposure levels, C57BL/6 mice exhibited pulmonary injury characterized by significant inflammation, oxidative stress, and cardiac damage. Notably, C57BL/6 mice showed free radical signals, indicating a distinct susceptibility profile. Immunodeficient non-obese diabetic Prkdc -/-/ Il2rg -/- (NPI) mice exhibited minimal biological responses to pulmonary injury, with little impact on the heart. These findings suggest a divergence in ozone-induced damage pathways in the two mouse types, leading to alterations in exhaled biomarkers. Integrating biomarker discovery with comprehensive biopathological analysis forms a robust foundation for targeted interventions to manage health risks posed by ozone exposure. [Display omitted] • PAI-TOFMS detects exhaled biomarkers of ozone-exposed mice with high sensitivity. • The impact of ozone varies distinctly between the heart and lungs in mice. • The immune responses are vital in ozone-related damage. • Free radicals in EBC are linked to ozone exposure and immune responses. • Exhaled breath analysis is a promising tool for monitoring ozone exposure. [ABSTRACT FROM AUTHOR]

Bronchitis is a common respiratory condition that can be acute or chronic, causing inflammation of the bronchial tubes. It is often caused by viral infections, but bacteria, irritants, and environmental factors can also contribute. Symptoms of acute bronchitis are similar to those of a cold or flu, while chronic bronchitis is characterized by a persistent cough. Treatment depends on the underlying cause and may involve medications, oxygen therapy, pulmonary rehabilitation, and quitting smoking. Practicing good hand hygiene, avoiding close contact with sick individuals, and protecting oneself from environmental irritants can help reduce the risk of bronchitis. [Extracted from the article]

[Display omitted] • ELP treatment attenuates airway inflammation and obstruction in lipopolysaccharide-induced chronic bronchitis rat. • ELP treatment improves metabolic pathway changes that caused by LPS challenge. • ELP could inhibit the TLR4 signaling pathways in LPS-induced Beas-2B cells and CB rats. Chronic bronchitis (CB), a type of chronic obstructive pulmonary disease (COPD), poses a significant global health burden owing to its high morbidity and mortality rates. Eucalyptol, limonene and pinene enteric capsules (ELPs) are clinically used as expectorants to treat various respiratory diseases, including CB, but their acting mechanisms remain unclear. In this study, we investigated the anti-CB effects of ELP in a rat model of lipopolysaccharide (LPS)-induced CB. The molecular mechanisms underlying its inhibitory effects on airway inflammation were further explored in LPS -stimulated Beas-2B cells. ELP was characterized using gas chromatography. The production of inflammatory mediators in bronchoalveolar lavage fluid (BALF) was determined using an enzyme-linked immunosorbent assay. The expression of MUC5AC, MUC5B, and p-p65 in the lung tissue was measured using immunohistochemical staining. The gene expression of inflammatory mediators was determined using qRT-PCR. The expression levels of the target proteins were detected by western blotting. Nuclear localization of p65 was determined using an immunofluorescence assay. Compared to the CB model rats, ELP-treated rats showed reduced airway resistance, inflammation, and goblet cell hyperplasia. In BALF, ELP decreased the levels of inflammatory mediators, including TNF-α, IL-6, MIP-1α, and CCL5. ELP also suppressed LPS -induced elevation of MUC5AC, MUC5B, and p-p65 in the lung tissue. The metabolic pathway changes caused by LPS challenge were improved by ELP treatment. In LPS -exposed Beas-2B cells, ELP treatment inhibited the expression of TNFA , IL6 , CCL5 , MCP1 , and MIP2A and decreased the phospho-levels of toll-like receptor 4 (TLR4) signaling-related proteins, including p-p38, p-JNK, p-ERK, p-TBK1, p-IKKα/β, p-IκB, p-p65, and p-c-Jun. ELP also hindered the nuclear translocation of p65, c-Jun, and IRF3. This study showed that ELP has a potential therapeutic effect in LPS-induced CB rat model, possibly by suppressing TLR4 signaling. These results justify the clinical use of ELP for the treatment of pulmonary inflammatory diseases. [ABSTRACT FROM AUTHOR]

Ambient air pollution increases the risk of respiratory mortality and morbidity, but evidence concerning effects of air pollution on chronic bronchitis (CB) is scarce. This study aimed to evaluate the associations of a set of air pollutants with the burden of CB, and to explore potential modifiers on the associations. In 2020, a total of 6,556,440 adults living in the Northwestern region of China were recruited. The Space-Time Extra-Trees model was employed to assess the annual average concentrations of six air pollutants for the three years (2017-2019) before 2020 , and subsequently allocated to the participants based on the latitude and longitude of their home addresses. We investigated the associations between the levels of various air pollutants and the odds of CB using generalized linear mixed models, and conducted multiple sensitivity analyses and subgroup analyses. The odds of CB displays an approximately linear association with particulate matter with aerodynamic diameter ≤2.5 μm (PM 2.5), particulate matter with aerodynamic diameter ≤10 μm (PM 10), while it shows a non-linear relationship with gaseous pollutants. In the adjusted model, the odds ratios and 95% confidence intervals for CB per 10 μg/m3 increase in PM 2.5 , PM 10 , and sulfur dioxide (SO 2) were 1.297 (1.262–1.332), 1.072 (1.064–1.080), and 2.587 (2.186–3.063), respectively. Furthermore, several additional sensitivity analyses demonstrated the stability of these associations. Subgroup analyses found that the aforementioned associations were greater among participants aged below 50 years old and those who smoked and had no leisure time exercise. Long-term exposure to ambient air pollutants may increase the odds of CB, especially among younger people and those with unhealthy lifestyles. [Display omitted] • Evidence concerning ambient air pollution and chronic bronchitis (CB) is limited. • We examined the association between air pollution and CB in northwestern China. • Exposure to particulate and gaseous pollutants was related to higher odds of CB. • Our findings may help develop individual-and population-level interventions to reduce CB burden. [ABSTRACT FROM AUTHOR]

The extracellular signals that initiate intracellular reactions are dispatched by the mitogen-activated protein kinases (MAPKs), which oversee a multitude of cellular activities. p38, Extracellular signal-regulated kinase (ERK), and c-Jun NH2-terminal kinase (JNK) are members of the vertebrate family of MAPKs, and each MAPK signaling pathway consists of a MAPK kinase (MAP3K), a MAPK kinase (MAP2K), and a MAPK. These signaling pathways orchestrate numerous cellular processes, including cell growth, survival, differentiation, and apoptosis. The emergence of various inflammatory respiratory diseases in humans has been linked to the dysregulation of MAPK signaling pathways. Conditions such as asthma, lung cancer, pulmonary fibrosis, and COPD are among the prevalent respiratory ailments where MAPK plays a pivotal role. Additionally, MAPK is implicated in infectious diseases, including COVID-19, pneumonia, and tuberculosis. COPD, asthma, emphysema, chronic bronchitis, and other inflammatory lung disorders highlight the significance of MAPK as a potential target for therapeutic development. Further studies are needed to delve into the molecular mechanisms by which the MAPK signaling pathway contributes to inflammatory lung disorders, representing an area that demands continued research. [ABSTRACT FROM AUTHOR]

Gleditsiae sinensis fructus Pills (GF) is a famous classical prescription, that is regularly combined with Jujubae fructus (JF) for the treatment of chronic bronchitis (CB) in the clinic. While the clinical efficacy of this combination prescription is clearly established, the active ingredients and molecular mechanisms remain unclear. To elucidate the mechanisms of action of Gleditsiae sinensis fructus Pills combined with Jujubae fructus (GF&JF) against CB based on network pharmacology and experimental verification. The potential targets of GF&JF involved in therapeutic activity against CB were predicted based on network pharmacology and an "ingredients-targets" network constructed. The Metascape database was used for Module, GO functional and KEGG signaling pathway enrichment analyses of potential targets. Molecular docking was applied to simulate the binding activities of key candidate active ingredients to core targets. For experimental verification, a CB model was established through smoking and nasal cavity drip of lipopolysaccharide. Related inflammatory factors, including TNF-α, TGF-β, IL-6 and IL-8 in serum, and IL-4 IL-8, IFN-γ and IL-10 in bronchoalveolar lavage fluid (BALF), were detected using ELISA. Hematoxylin and eosin (H&E) and Masson staining were performed to observe pathological changes in lung and tracheal tissue. The expression of related proteins and mRNAs in the lung tissue were detected using immunohistochemistry (IHC), quantitative real-time PCR, and western blot. In network pharmacology, 36 common targets of GF&JF for CB were screened and the key targets and main signaling pathways identified. The active ingredients quercetin and stigmasterol in GF&JF had more targets for CB, which displayed good binding activity to IL-6, VEGFA, and EGFR, as established from molecular docking results. In vivo , GF&JF effectively inhibit the inflammatory response in CB mice and improved pathological changes in lung and tracheal tissue. In terms of the key proteins of the AGE-RAGE signaling pathway, GF&JF induced significant down-regulation of IL-6, ICAM-1, VCAM-1, EGFR, CASPASE-3, AGEs and RAGE proteins in lung tissue as well as mRNA expression of IL-6, ICAM-1, VCAM-1, EGFR, AGEs and RAGE. The GF&JF combination exerts a good therapeutic effect in CB model mice, which may be attributed to inhibition of the inflammatory response as well as regulation on the expression of AGE-RAGE signaling pathway. In addition, quercetin and stigmasterol appear to be the main active ingredients of GF&JF in the treatment of CB. [Display omitted] • GF was described in "Jingui Yaolue" by Zhongjing Zhang in the Han Dynasty. • Classical prescription GF&JF was an ancient prescription mainly used for chronic bronchitis. • GF&JF has a better therapeutic effect on CB, which may be related to regulating the expression of AGE-RAGE signaling pathway. [ABSTRACT FROM AUTHOR]

Zhisou Powder (ZP), one of the most common prescriptions in traditional Chinese medicine, has been widely used in the treatment of acute or chronic bronchitis and chronic cough. The ZP was composed of Ziwan (Aster tataricus L. f.), Jiegeng (Platycodon grandiflorus (Jacq.) A. DC.), Jingjie (Nepeta cataria L.), Baibu (Stemona sessilifolia (Miq.) Miq.), Baiqian (Vincetoxicum glaucescens (Decne.) C. Y. Wu & D. Z. Li), Chenpi (Citrus × aurantium f. deliciosa (Ten.) M. Hiroe) and Gancao (Glycyrrhiza uralensis Fisch. ex DC.), with plant names among it checked with MPNS (http://mpns.kew.org). But until now, the key active components and targets of ZP, and related mechanism of ZP in the treatment of chronic bronchitis (CB) remain unclear. This study combined UPLC-Q-Exactive-Orbitrap-MS, network pharmacology, metabonomics with experiment verification to explore potential mechanism of ZP in the treatment of CB. UPLC-Q-Exactive-Orbitrap-MS was performed to analyze the chemical components of ZP. The potentially effective components, attractive targets and critical signaling pathways of Zhisou Powder in the treatment of CB were screened by UPLC-Q-Exactive-Orbitrap-MS combined with network pharmacology. Additionally, the CB model rats induced by SO 2 were used to evaluate the anti-chronic bronchitis activity of ZP in vivo. The pulmonary pathology was determined by hematoxylin-eosin staining. Meanwhile, PI3K/Akt/HIF-1α/VEGFA signaling pathway predicted from network pharmacology was verified by Western blot and RT-PCR. Lastly, the metabolic changes of arachidonic acid (AA) in ZP-treated rats were quantitatively analyzed by LC-MS targeted metabonomics, and the proteins expression involved in AA metabolic pathway were detected by immunohistochemistry, immunofluorescence and Western blot. The main active components of ZP in the treatment of CB selected by network pharmacology and UPLC-Q-Exactive-Orbitrap-MS technology were quercetin, kaempferol, luteolin, galangin, isorhamnetin, naringenin, nobiletin, formononetin and so on. The core targets of these components were predicted to be TP53, TNF, IL-6, VEGFA, CASP3, IL-1β, JUN, PTGS2. Enrichment of KEGG pathway analysis found that PI3K/Akt/HIF-1α/VEGFA signaling pathway might play a key role in the treatment of CB with ZP. The in vivo study showed that ZP significantly improved the pathological changes of SO 2 -treated lung tissue and inhibited the activation of PI3K/Akt/HIF-1α/VEGFA signaling pathway. The changes of AA and its metabolites in vivo were studied by targeted metabonomics, and it showed that ZP could reprogram the disorder of AA metabolism which contributed to the treatment of CB with ZP. ZP displayed good therapeutic effect on CB model rats through inhibiting PI3K/Akt/HIF-1α/VEGFA signaling pathway to exhibit anti-inflammatory effect and reprogramming disordered metabolic pathway of arachidonic acid. [Display omitted] [ABSTRACT FROM AUTHOR]