ObjectiveTo systematically evaluate the methodological quality and measurement properties of traditional Chinese medicine （TCM） syndrome efficacy evaluation scales， and to provide evidence-based references for selecting high-quality assessment tools in TCM clinical practice. MethodsChina National Knowledge Infrastructure （CNKI）， Wanfang Data， VIP Database， Chinese Biomedical Literature Database （CBM）， PubMed， the Cochrane Library， Embase， and Web of Science were searched from inception to April 2， 2025， for studies evaluating the measurement properties of TCM syndrome efficacy evaluation scales. Data were extracted， and the methodological quality and measurement properties of the included scales were assessed according to the consensus-based standards for the selection of health measurement instruments （COSMIN）. Recommendation levels were formulated based on the grading of evidence. ResultsA total of 46 studies were included， involving 22 generic syndrome efficacy evaluation scales and 24 disease-specific syndrome efficacy evaluation scales. None of the scales reported cross-cultural validity or measurement error. According to the recommendation grades， 2 scales met Grade A recommendations and are suggested for clinical use； 38 scales were classified as Grade B， indicating potential applicability but requiring further validation； and 6 scales were classified as Grade C， suggesting the need for further refinement. ConclusionExisting TCM syndrome efficacy evaluation scales exhibit substantial variability in methodological quality， incomplete reporting of measurement properties， and insufficient attention to scale revision. Future efforts should emphasize standardized design in the development of TCM syndrome scales， strengthen validation procedures for key measurement properties， and prioritize dynamic revision of scales， thereby providing high-quality tools to support the precise evaluation of syndrome efficacy.

By systematically reviewing the concept evolution of pre-chronic obstructive pulmonary disease （pre-COPD） and the research status of traditional Chinese medicine （TCM）， as well as considering the clinical practice， this paper puts forward the strategies for the prevention and treatment of pre-COPD with TCM. These strategies include identifying high-risk groups by combining TCM syndrome and constitution， advocating the principle of "treating disease before it arises" and promoting the combination of syndrome differentiation and constitution evaluation to achieve individualized intervention， promoting collaboration between TCM and western medicine， supported by digital and intelligent technologies， to establish a whole-process management mode of "hospital-community-family". The aim is to realize the early diagnosis， early intervention and whole-process management of pre-COPD， thereby helping reduce the incidence of COPD.

ObjectiveTo investigate the incidence rate of post-endoscopic retrograde cholangiopancreatography （ERCP） pancreatitis （PEP） in patients with difficult common bile duct intubation undergoing pancreatic duct stenting during surgery， as well as the effect of pancreatic duct stenting in the prevention and treatment of PEP， and to provide a basis for clinical treatment. MethodsA retrospective analysis was performed for the clinical data of 186 patients with biliary tract disease who underwent initial ERCP and had difficult common bile duct intubation in The First Affiliated Hospital of Zhengzhou University from January 2016 to December 2024， and according to the condition of pancreatic duct stenting， the patients were divided into control group with 73 patients （without pancreatic duct stenting）， 5Fr-5 cm stent group with 67 patients， and 7Fr-5 cm stent group with 46 patients. The three groups were compared in terms of baseline data， intraoperative procedures， and postoperative outcomes. A one-way analysis of variance was used for comparison of normally distributed continuous data between multiple groups， and the least significant difference t-test was used for further comparison between two groups； the Kruskal-Wallis H rank sum test was used for comparison of non-normally distributed continuous data between multiple groups， and the Dunn method was used for further comparison between two groups； the chi-square test or the Fisher’s exact test was used for comparison of categorical data between groups. The Logistic regression analysis was used to investigate the influencing factors for PEP in patients with difficult intubation during ERCP. ResultsThe overall incidence rate of PEP was 12.37% （23/186）. Compared with the 5Fr-5 cm stent group and the 7Fr-5 cm stent group， the control group had a significantly higher incidence rate of PEP， a significantly higher score of postoperative abdominal pain， and a significantly longer length of postoperative hospital stay （all P0.01）， and 55.56% of the patients in the control group had moderate-to-severe PEP. The univariate Logistic regression analysis showed that intradiverticular papilla， double guide wire intubation， needle knife precut， the application of basket and balloon for removal of common bile duct stones， intraoperative biopsy， pancreatic duct stenting， intubation time≤10 minutes， frequency of intubation≤5 times， preoperative CRP≤5 mg/L were influencing factors for PEP （all P0.05）， and the multivariate Logistic regression analysis showed that intraoperative pancreatic duct stenting， needle knife precut， and intraoperative biopsy were independent influencing factors for the onset of PEP （all P0.05）. ConclusionPancreatic duct stenting during ERCP can effectively reduce the risk of PEP in patients with difficult intubation， while needle knife precut and intraoperative biopsy can increase the risk of PEP in patients with difficult intubation.

OBJECTIVES: To investigate pharmacologically active components of Yiqi Zishen Formula (YZF) and their mechanisms for alleviating airway inflammation in mice with chronic obstructive pulmonary disease (COPD). METHODS: Ultra-high-performance liquid chromatography coupled with quadrupole-orbitrap mass spectrometry was employed to characterize the chemical components in YZF and YZF-medicated rat serum. A compound-disease target network was constructed based on serum components of YZF to screen the key pathways and targets using enrichment analysis. A mouse model of cigarette smoke-induced COPD was used to evaluate the anti-inflammatory effect of YZF and validate the expression of key proteins in network pharmacology-enriched pathways. Fifty male C57BL/6J mice were randomized equally into control group, COPD model group, high- and low-dose YZF treatment groups, and N-acetylcysteine treatment group. Pulmonary function of the mice was assessed using whole-body plethysmography, and lung histopathology, alveolar structure, and airway remodeling were analyzed using HE staining. The levels of IL-1β, IL-6, and TNF‑α in bronchoalveolar lavage fluid (BALF) were determined with ELISA, and pulmonary expressions of PI3K, Akt, phosphorylated Akt (p-Akt), p65, and phosphorylated p65 (p-p65) were detected using immunohistochemistry. RESULTS: We identified a total of 156 chemical components (including 26 flavonoids or flavonoid glycosides, 27 alkaloids, and 11 saponins) in YZF and 43 prototype components in medicated rat serum. Network pharmacology revealed 704 YZF-related targets and 1199 COPD-associated targets. Integrated analysis suggested that the anti-COPD effects of YZF were associated with the PI3K-Akt signaling pathway. In mouse models of COPD, YZF treatment significantly increased mean alveolar number and peak expiratory flow (P<0.05), reduced mean linear intercept, bronchial wall thickness, lung coefficient, and BALF cytokine levels, and suppressed the expressions of PI3K, Akt, p-Akt, p65, and p-p65 in the lung tissues. CONCLUSIONS YZF alleviates COPD symptoms and airway inflammation in mice possibly by inhibiting the PI3K/Akt/NF‑κB pathway through its multiple components that interact with multiple targets.
Animals ; Pulmonary Disease, Chronic Obstructive/metabolism* ; Drugs, Chinese Herbal/therapeutic use* ; Signal Transduction/drug effects* ; Male ; Mice, Inbred C57BL ; Mice ; Proto-Oncogene Proteins c-akt/metabolism* ; Phosphatidylinositol 3-Kinases/metabolism* ; NF-kappa B/metabolism* ; Inflammation/drug therapy* ; Rats

Granulation tissue hyperplasia after tracheotomy is a common clinical complication. Endoscopic treatment can temporarily relieve airway obstruction， however， it is associated with a high recurrence rate and poor long-term prognosis. Based on the traditional Chinese medicine （TCM） Kenang （窠囊） theory and combined with modern pathological mechanisms， this paper explores its correlation with the pathogenesis of post-tracheotomy granulation tissue hyperplasia. Drawing from clinical experience in applying the Kenang theory for treatment， this paper proposes that the fundamental pathogenesis of this condition lies in qi deficiency and organ dysfunction， while phlegm and blood stasis interlocking serve as the symptomatic manifestations. The treatment focuses on resolving phlegm and promoting blood circulation， dispersing nodules and eliminating stagnation， regulating qi flow， and reinforcing the body's vital energy while expelling pathogenic factors. This approach aims to dissolve phlegm and blood stasis， dissipate the Kenang， and ultimately prevent and treat granulation tissue hyperplasia.

Objective To provide methodological examples for related research,the influencing factors of the evolution of Qi deficiency syndrome in chronic obstructive pulmonary disease(COPD)based on a nonlinear mixed effects model was explored.Methods A research questionnaire on the influencing factors of the evolution of Qi deficiency syndrome in chronic obstructive pulmonary disease was developed,and clinical data of 650 COPD patients on the 1st and 14th day of acute exacerbation,the 1st and 28th day of risk window,the first day of stable period,and the 90th day were dynamically collected from 10 tertiary hospitals across the country.8 baseline data including gender and age were collected through the PROC NLMIXED process by SAS 9.4 software.Coronary heart disease,diabetes and hypertension accounted for the highest proportion.Nine concurrent syndromes including wind cold syndrome and phlegm heat syndrome were used as fixed effects,and individual level was used as random effects to gradually fit the model and screen the influencing factors of Qi deficiency syndrome in the entire process of disease occurrence and development.Results A total of 637 eligible cases were included,and clinical datas were dynamically collected on the 1st and 14th day of acute exacerbation,the 1st and 28th day of the risk window,the 1st and 90th day of the stable period.It was found that the number of acute exacerbations,alcohol consumption,concomitant hypertension,coronary heart disease,blood stasis syndrome,yin deficiency syndrome,yang deficiency syndrome,6-minute walking distance,and the modified Medical Research Council Dyspnea Questionnaire(mMRC)had an impact on the evolution of Qi deficiency syndrome in the previous year(P<0.05).Conclusion The use of a nonlinear mixed effects model revealed the relevant factors affecting the evolution of Qi deficiency syndrome from complex multi temporal dynamic data,providing methodological references for other related studies.

Objective To investigate pharmacologically active components of Yiqi Zishen Formula(YZF)and their mechanisms for alleviating airway inflammation in mice with chronic obstructive pulmonary disease(COPD).Methods Ultra-high-performance liquid chromatography coupled with quadrupole-orbitrap mass spectrometry was employed to characterize the chemical components in YZF and YZF-medicated rat serum.A compound-disease target network was constructed based on serum components of YZF to screen the key pathways and targets using enrichment analysis.A mouse model of cigarette smoke-induced COPD was used to evaluate the anti-inflammatory effect of YZF and validate the expression of key proteins in network pharmacology-enriched pathways.Fifty male C57BL/6J mice were randomized equally into control group,COPD model group,high-and low-dose YZF treatment groups,and N-acetylcysteine treatment group.Pulmonary function of the mice was assessed using whole-body plethysmography,and lung histopathology,alveolar structure,and airway remodeling were analyzed using HE staining.The levels of IL-1β,IL-6,and TNF-α in bronchoalveolar lavage fluid(BALF)were determined with ELISA,and pulmonary expressions of PI3K,Akt,phosphorylated Akt(p-Akt),p65,and phosphorylated p65(p-p65)were detected using immunohistochemistry.Results We identified a total of 156 chemical components(including 26 flavonoids or flavonoid glycosides,27 alkaloids,and 11 saponins)in YZF and 43 prototype components in medicated rat serum.Network pharmacology revealed 704 YZF-related targets and 1199 COPD-associated targets.Integrated analysis suggested that the anti-COPD effects of YZF were associated with the PI3K-Akt signaling pathway.In mouse models of COPD,YZF treatment significantly increased mean alveolar number and peak expiratory flow(P<0.05),reduced mean linear intercept,bronchial wall thickness,lung coefficient,and BALF cytokine levels,and suppressed the expressions of PI3K,Akt,p-Akt,p65,and p-p65 in the lung tissues.Conclusion YZF alleviates COPD symptoms and airway inflammation in mice possibly by inhibiting the PI3K/Akt/NF-κB pathway through its multiple components that interact with multiple targets.

Objective Cigarette smoke(CS)exposure combined with Klebsiella pneumoniae(KP)infection in mice was used to establish a model of chronic obstructive pulmonary disease(COPD)to investigate the mechanism of airway remodeling.Methods Male BALB/c mice were randomly divided into a Control group,CS group,KP group,and CS+KP group.The mice were exposed to CS,KP,and CS+KP from weeks 1 to 8,and were sacrificed in weeks 4,8,16,and 24.MV,Penh,MLI,MAN,and changes in lung pathological structure were detected.The expression levels of IL-1β and TNF-α in lung tissue were detected by ELISA.Collagen deposition was observed by Masson staining and immunohistochemistry.α-SMA and TGF-β1 expression in lung tissue was detected by immunofluorescence.Human bronchial epithelioid cells(16HBE)were also stimulated by CS and lipopolysaccharide(LPS)in vitro,and the expression levels of airway epithelial junction proteins,autophagy-related protein,and mTOR signaling proteins were detected.Results Compared with the Control group,the CS+KP group mice had significantly decreased MV from weeks 4 to 24(P＜0.05 or P＜0.01)and significantly increased Penh from weeks 8 to 24(P＜0.05 or P＜0.01);while the CS group had markedly decreased MV and markedly increased Penh from weeks 8 to 16(P＜0.05 or P＜0.01).Compared with the Control group,massive inflammatory cell infiltration,alveolar wall thickening,alveolar rupture and fusion,and airway wall thickening were observed by HE staining in CS+KP group from weeks 4 to 24.The CS+KP group mice had significantly decreased MAN and significantly increased MLI,IL-1β and TNF-α in their lung tissue from weeks 4 to 24(P＜0.05 or P＜0.01).The aforementioned inflammation and tissue damage were observed in the CS group and the KP group from week 8 to 16.Compared with the Control group,COL Ⅰ,COL Ⅲ,α-SMA,and TGF-β1 were significantly increased in lung tissue of mice in the CS+KP group from weeks 8 to 16(P＜0.01);COL Ⅰ was significantly increased in the CS group and KP group from weeks 8 to 16(P＜0.01).In addition,increased E-cad and decreased N-cad(P＜0.05);significantly decreased LC3B and Beclin-1(P＜0.05);and significantly increased p-mTORC1,p-P70-S6K,and p-4E-BP1 expression were observed in 16HBE cells exposed to CS and LPS(P＜0.05 or P＜0.01).Conclusion Pulmonary functional decline,pathological changes in lung tissue,and airway remodeling appeared to occur early and persist in COPD mice induced by CS and KP.The mechanisms may be related to the activation of mTORC1 signaling pathway and subsequent inhibition of autophagy.

AIM:To investigate the effects of the Qingfei-Jiedu-Huatan formula(QJHF)on damage to the lung vascular endothelial barrier induced by Klebsiella pneumoniae in mice with severe pneumonia,as well as to elucidate its underlying mechanisms.METHODS:Fifty-one C57BL/6J mice were randomly divided into control group(n=6),model group(n=15),QJHF group(n=15),and ceftriaxone sodium(CRO)group(n=15).Severe pneumonia was in-duced in the mice by a single tracheal intubation with 50 μL of 1×1011 CFU/mL Klebsiella pneumoniae on day 0.Six hours after modeling,the mice in QJHF and CRO groups received their respective treatments,while those in control and model groups were administered an equal volume of saline.All mice were sacrificed on day 3 after the end of gavage.Lung histo-pathological changes were assessed using hematoxylin-eosin(HE)staining.Levels of tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β),and IL-6 in lung tissues were measured by enzyme-linked immunosorbent assay(ELISA).Flow cytometry was used to detect CD11b+Ly6g+cells in bronchoalveolar lavage fluid(BALF).Proteomics and network pharma-cology analyses were conducted to elucidate the mechanisms of drug action.Western blot was conducted to assess the ex-pression levels of vascular endothelial cadherin(VE-cadherin),zonula occludens-1(ZO-1),occludin,vascular endothe-lial growth factor(VEGF),P38 mitogen-activated protein kinase(P38),and phosphorylated P38(p-P38)in lung tis-sues.RESULTS:Treatment with QJHF significantly attenuated the symptoms such as mental status and respiratory dis-tress,reduced mortality,mitigated lung tissue lesions,and decreased levels of IL-6,TNF-α,IL-1β,as well as BALF to-tal protein concentration,total cell count and neutrophil content in a mouse model of severe pneumonia(P＜0.05 or P＜0.01).Additionally,QJHF increased the expression of VE-cadherin,ZO-1 and occludin proteins in lung tissues.Pro-teomic analysis demonstrated that QJHF modulated the expression of 129 proteins in the lung tissues of mice suffering from severe pneumonia.Network pharmacology identified 328 potential targets associated with 14 major bioactive components of QJHF and 1 665 genes related to severe pneumonia,with 125 overlapping genes between the two datasets.The construc-tion of a protein-protein interaction(PPI)network,along with Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)enrichment analyses of the regulated proteins and overlapping genes,indicated that QJHF primarily in-fluenced the PI3K-Akt,MAPK and Rap1 signaling pathways,as well as VEGFR.Western blot analysis showed that QJHF significantly inhibited the expression of VEGF and P38 in lung tissues(P＜0.05 or P＜0.01).CONCLUSION:Treatment with QJHF attenuates severe pneumonia in mice,potentially by inhibiting VEGF/P38 signaling to protect the vascular endothelial barrier.