Chronic obstructive pulmonary disease（COPD） is a common chronic respiratory disorder frequently accompanied by diaphragmatic dysfunction during its course， which significantly increases respiratory burden and impairs quality of life. As the primary inspiratory muscle， the diaphragm is prone to fatigue， atrophy， inflammation， and fibrosis during the long-term progression of COPD. Its pathological mechanisms involve multiple pathways such as inflammatory responses， oxidative stress， mitochondrial dysfunction， apoptosis， ion channel abnormalities， epigenetic regulation， autophagy disorder， and protein metabolism imbalance. In recent years， traditional Chinese medicine（TCM） has demonstrated multi-targeted and systemic regulatory advantages in improving diaphragmatic function in COPD. However， related studies remain fragmented， and integrated mechanistic understanding is lacking. This paper focuses on the mechanism-target-TCM intervention framework， systematically summarizing the molecular mechanisms of diaphragmatic dysfunction， while incorporating the TCM theory of Zongqi（ancestral Qi）. It highlights the therapeutic effects of Chinese herbal formulas， single herbs， and active components in modulating inflammation， oxidative stress， mitochondrial function， ion channels， epigenetic processes， autophagy， and protein homeostasis. Additionally， the review outlines existing challenges， including insufficient study volume， unbalanced selection of herbal prescriptions， limited mechanistic depth， inconsistent disease models and experimental designs， lack of standardized diaphragmatic function assessment， and weak clinical validation. Future research should strengthen the integration of TCM and modern medicine， identify additional therapeutic targets， deepen mechanistic research， and establish unified and standardized experimental systems to advance the theoretical foundation and clinical application of TCM in the prevention and treatment of COPD-related diaphragmatic dysfunction.

Chronic obstructive pulmonary disease（COPD） is a common chronic respiratory disorder frequently accompanied by diaphragmatic dysfunction during its course， which significantly increases respiratory burden and impairs quality of life. As the primary inspiratory muscle， the diaphragm is prone to fatigue， atrophy， inflammation， and fibrosis during the long-term progression of COPD. Its pathological mechanisms involve multiple pathways such as inflammatory responses， oxidative stress， mitochondrial dysfunction， apoptosis， ion channel abnormalities， epigenetic regulation， autophagy disorder， and protein metabolism imbalance. In recent years， traditional Chinese medicine（TCM） has demonstrated multi-targeted and systemic regulatory advantages in improving diaphragmatic function in COPD. However， related studies remain fragmented， and integrated mechanistic understanding is lacking. This paper focuses on the mechanism-target-TCM intervention framework， systematically summarizing the molecular mechanisms of diaphragmatic dysfunction， while incorporating the TCM theory of Zongqi（ancestral Qi）. It highlights the therapeutic effects of Chinese herbal formulas， single herbs， and active components in modulating inflammation， oxidative stress， mitochondrial function， ion channels， epigenetic processes， autophagy， and protein homeostasis. Additionally， the review outlines existing challenges， including insufficient study volume， unbalanced selection of herbal prescriptions， limited mechanistic depth， inconsistent disease models and experimental designs， lack of standardized diaphragmatic function assessment， and weak clinical validation. Future research should strengthen the integration of TCM and modern medicine， identify additional therapeutic targets， deepen mechanistic research， and establish unified and standardized experimental systems to advance the theoretical foundation and clinical application of TCM in the prevention and treatment of COPD-related diaphragmatic dysfunction.

Objective To compare the impact of NaClO and EDTA pretreatment on the enamel surfaces pore exposure rate,resin in-filtration effectiveness and shear bond strength between the enamel white spot lesions(WSLs)and resin composite.Methods A total of 104 sound premolars were selected for the study.4 mm×4 mm×2 mm enamel blocks from 64 sound premolars were cut in the center of the buccal surfaces of the teeth.All blocks were randomly divided into five groups:group SE(sound enamels as negative control);group DE(enamel blocks demineralised as positive control);group RI(resin infiltration);group N/RI(5.25％NaClO pretreatment and resin infiltration)and group E/RI(17％EDTA pretreatment and resin infiltration).The pore exposure rate of enamel surfaces and resin penetration depths were observed by scanning electron microscopy(SEM)and confocallaser scanning microscopy(CLSM)in each group.The remaining 40 premolars were cut from the cervical roots and the residual crowns were embedded in self-condensing resin ma-terial(buccal surfaces of the enamel exposed only).According to the grouping information,the samples were given the corresponding pretreatments and resin infiltration respectively and were bonded with a cylindrical resin cylinder on the buccal enamel surface for shear bond test.The shear bond strength and fracture modes were recorded and analyzed in each group.Results Compared to group RI,the pore exposure rate of the enamel surface,resin penetration depths,and percentage of resin penetration area in the N/RI and E/RI groups were significantly increased(P＜0.05).The shear bond strength of the samples in group SE was the highest,and the lowest in group DE.Compared to group DE,the shear bond strength in groups RI,N/RI,and E/RI was significantly increased(P＜0.05).Con-clusion Enamel surface pretreatment with 5.25％NaClO or 17％EDTA has been demonstrated to effectively enhance the enamel pore exposure rate,resin penetration depth and the shear bond strength between WSLs and resin composite.

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 explore the effects and potential molecular mechanisms of blocking cannabinoid receptor 1(CB1)in acute lung injury(ALI)in mice.Methods·Forty mice were randomly divided into blank control group,AM281(CB1 antagonist)control group,lipopolysaccharide(LPS)group,and LPS+AM281 group,with ten mice in each group.ALI models were induced by LPS.The pathological manifestations of lung tissues were observed in each group of mice by hematoxylin and eosin(H-E)staining and the inflammation scores were calculated.The mRNA levels of M1 markers[tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β),IL-12]and M2 markers[arginase(Arg),mannose receptor,C type 2(Mrc2),macrophage galactose-type lectin 1(Mgl1)]in lung macrophages were measured by reverse transcription and real-time fluorescence quantitative polymerase chain reaction(qPCR).Human myeloid leukemia monocytes THP-1 cells were cultured in vitro,and the expression of CB1 and CB2 in THP-1 cells was detected by immunofluorescence.After further blocking CB1 and inhibiting the Gαi/o/RhoA signaling pathway,the mRNA levels of M1 markers were assessed.Results·The LPS group showed significant lung tissue damage and a significant increase in inflammation scores in mice.After blocking CB1,compared with the LPS group,the LPS+AM281 group of mice showed improvements in lung injury,manifested as improved congestion of alveolar wall capillaries,reduced infiltration of inflammatory cells in the lung interstitium and alveolar cavity,and a decreased inflammation score(P=0.007).Compared with the control group,the levels of M1 marker in the lung tissue of the LPS group were upregulated,while the polarization of macrophages changed and the M1/M2 ratio was reversed after blocking CB1(all P<0.05).In vitro studies found that macrophages expressed CB1 and CB2.Activation of CB1 by arachidonyl-2-chloroethylamide(ACEA)upregulated the expression of M1 markers.Blocking CB1 and selectively inhibiting Gαi/o/RhoA signaling significantly downregulated M1 markers(all P<0.05).Conclusion·CB1 promotes the polarization of macrophage towards the M1 phenotype through the Gαi/o/RhoA signaling pathway in ALI,and blocking CB1 can improve lung injury.

Objective"Red butterfly sore","yin-yang toxin"and"Bi disease"are different Chinese medicine diagnoses of systemic lupus erythematosus(SLE).It is not clear whether there are biological differences between these three types of Chinese medicine diagnoses.The aim of this study was to compare the different TCM diagnoses of SLE patients from the perspective of lymphocyte subsets and cytokines.Methods Patients diagnosed with SLE in our hospital from June 1,2021 to December 1,2023 were retrospectively collected,and the differences of T cell subsets,NK cells,B lymphocytes and Th1,Th2 and Th17 cytokines among different groups were compared by one-way ANOVA or nonparametric test.As well as differences in laboratory test indicators such as erythrocyte sedimentation rate(ESR),C-reactive protein(CRP),immunoglobulin,and complement,receiver operating characteristic curve(ROC curve)was used to analyze the value of these indexes in the differential diagnosis of different types of SLE.Results From June 1,2021 to December 1,2023,291 patients diagnosed with SLE in our hospital for the first time were collected,and 104 cases meeting the exclusion criteria of this study were included,including 31 cases of red butterfly sores,30 cases of yin-yang toxin and 43 cases of BI disease.The absolute number and percentage of CD8+T cells,interleukin-10(IL-10)content and tumor necrosis factor α(TNF-α)content were different among the three groups of SLE patients diagnosed by different Chinese medicine,and the absolute number of CD8+T cells in the red butterfly sore group was significantly higher than that in the yin-yang toxicities group(P=0.039)and the disease group(P=0.008).CD8+T cell percentage in red butterfly sore group was significantly higher than that in yin-yang toxin group(P=0.014)and disease group(P=0.004),IL-10 and TNF-α levels in red butterfly sore group were significantly lower than those in disease group(P=0.015,P=0.036),and ROC curve analysis showed that,the absolute number and percentage of CD8+T cells can effectively distinguish red butterfly sores from yin-yang toxins(AUC=0.65,AUC=0.61,P<0.05),and the absolute number and percentage of CD8+T cells,IL-10 and TNF-α can effectively distinguish red butterfly sores from diseases(AUC=0.68,AUC=0.66,P<0.01,AUC=0.67,AUC=0.64,P<0.05).Conclusion Immune lymphocyte subtypes,cytokines,especially the absolute number and percentage of CD8+T cells,IL-10 and TNF-α may play an important role in the identification of different TCM diagnosis of SLE.

Objective·To explore the effects and potential molecular mechanisms of blocking cannabinoid receptor 1(CB1)in acute lung injury(ALI)in mice.Methods·Forty mice were randomly divided into blank control group,AM281(CB1 antagonist)control group,lipopolysaccharide(LPS)group,and LPS+AM281 group,with ten mice in each group.ALI models were induced by LPS.The pathological manifestations of lung tissues were observed in each group of mice by hematoxylin and eosin(H-E)staining and the inflammation scores were calculated.The mRNA levels of M1 markers[tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β),IL-12]and M2 markers[arginase(Arg),mannose receptor,C type 2(Mrc2),macrophage galactose-type lectin 1(Mgl1)]in lung macrophages were measured by reverse transcription and real-time fluorescence quantitative polymerase chain reaction(qPCR).Human myeloid leukemia monocytes THP-1 cells were cultured in vitro,and the expression of CB1 and CB2 in THP-1 cells was detected by immunofluorescence.After further blocking CB1 and inhibiting the Gαi/o/RhoA signaling pathway,the mRNA levels of M1 markers were assessed.Results·The LPS group showed significant lung tissue damage and a significant increase in inflammation scores in mice.After blocking CB1,compared with the LPS group,the LPS+AM281 group of mice showed improvements in lung injury,manifested as improved congestion of alveolar wall capillaries,reduced infiltration of inflammatory cells in the lung interstitium and alveolar cavity,and a decreased inflammation score(P=0.007).Compared with the control group,the levels of M1 marker in the lung tissue of the LPS group were upregulated,while the polarization of macrophages changed and the M1/M2 ratio was reversed after blocking CB1(all P<0.05).In vitro studies found that macrophages expressed CB1 and CB2.Activation of CB1 by arachidonyl-2-chloroethylamide(ACEA)upregulated the expression of M1 markers.Blocking CB1 and selectively inhibiting Gαi/o/RhoA signaling significantly downregulated M1 markers(all P<0.05).Conclusion·CB1 promotes the polarization of macrophage towards the M1 phenotype through the Gαi/o/RhoA signaling pathway in ALI,and blocking CB1 can improve lung injury.

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.

ObjectiveTo clarify the graded quantitative diagnostic characteristics of lung qi deficiency syndrome in chronic obstructive pulmonary disease （COPD） based on latent class analysis combined with a hidden structure model. MethodsClinical data， including the four diagnostic methods of traditional Chinese medicine （TCM）， were collected from 745 COPD patients with lung qi deficiency syndrome. Latent class modeling was performed using R 4.1.2 software， and each patient was classified into one of three severity categories （mild， moderate， or severe） based on probabilistic parameterization， parameter estimation， and model fitting. A database was established for different severity levels of lung qi deficiency syndrome. Based on this， Lantern 5.0 software was used to construct hidden structure models for mild， moderate， and severe lung qi deficiency syndrome， and syndrome differentiation rules were developed through comprehensive clustering. ResultsA latent class model was constructed using 28 symptoms and signs with a frequency greater than 10%. Considering TCM theory and model simplicity， the optimal model was determined when the number of latent classes was three， categorizing lung qi deficiency syndrome into mild （298 cases）， moderate （164 cases）， and severe （283 cases）. Hidden structure models were separately developed for each severity level， and syndrome differentiation rules were established. A comparison of common symptoms in the syndrome differentiation rules for mild and moderate lung qi deficiency syndrome showed no statistically significant differences in diagnostic values and weights （P＞0.05）， leading to their combined analysis and the development of a unified syndrome differentiation rule. Value and weight of quantitative diagnosis of mild-to-moderate lung qi deficiency syndrome were as followed： shortness of breath （diagnostic value 9.3， diagnostic weight 86.92%）， dyspnea on exertion （8.2， 76.64%）， low voice and reluctance to speak （6.7， 62.62%）， poor appetite （4.0， 37.38%）， loose stools （4.0， 37.38%）， weak cough sound （2.9， 27.10%）， wheezing （2.3， 21.50%）， fatigue （1.8， 16.82%）， spontaneous sweating （1.7， 15.89%）， susceptibility to colds （1.6， 14.95%）， swollen tongue （1.4， 13.08%）， teeth marks on the tongue edge （1.2， 11.21%）， deep pulse （1.6， 14.95%）， with a diagnostic threshold of 10.3. Value and weight of quantitative diagnosis of severe lung qi deficiency syndrome were as followed： weak cough sound （15.1， 61.13%）， soreness and weakness of the waist and knees （12.6， 51.01%）， shortness of breath （11.1， 44.94%）， low voice and reluctance to speak （8.3， 33.60%）， frequent nocturia （6.1， 24.70%）， spontaneous sweating （3.7， 14.98%）， susceptibility to colds （3.5， 14.17%）， teeth marks on the tongue edge （7.8， 31.58%）， pale tongue body （1.9， 7.69%）， white tongue coating （5.5， 22.27%）， thin pulse （1.5， 6.07%）， with a diagnostic threshold of 23.7. ConclusionThe combination of latent class analysis and a hideen structure model effectively clarified the graded quantitative diagnostic characteristics of lung qi deficiency syndrome， providing a reference for the quantitative diagnosis of other fundamental syndromes in TCM.

ObjectiveTo investigate the expression levels of miR-128-3p， SIRT1， and AMPK in the peripheral blood of patients with type 2 diabetes mellitus （T2DM） comorbid with nonalcoholic fatty liver disease （NAFLD）， as well as the role of miR-128-3p in predicting NAFLD in T2DM patients. MethodsA total of 80 patients with T2DM who were hospitalized in The First Affiliated Hospital of Anhui University of Chinese Medicine from September 2022 to August 2023 were enrolled and divided into T2DM group with 40 patients and NAFLD group with 40 patients， and according to the NAFLD fibrosis score （NFS）， the patients were further divided into progressive liver fibrosis group with 16 patients and non-progressive liver fibrosis group with 64 patients. General data and biochemical parameters were collected； quantitative real-time PCR was used to measure the mRNA expression levels of miR-128-3p， SIRT1， and AMPK in peripheral blood， and Western blot was used to measure the protein expression levels of SIRT1 and AMPK. The independent-samples t test was used for comparison of normally distributed data between two groups， and the Mann-Whitney U test was used for comparison of data with skewed distribution between two groups； the chi-square test was used for comparison of categorical data between two groups. The logistic regression analysis was used to identify the influencing factors for the presence of NAFLD and progressive liver fibrosis， and the receiver operating characteristic （ROC） curve analysis was used to determine the optimal cut-off value of miR-128-3p for predicting NAFLD. ResultsThere were significant differences between the NAFLD group and the non-NAFLD group in body mass index， fasting plasma glucose， glycated hemoglobin， fasting insulin， fasting C-peptide， alanine aminotransferase （ALT）， aspartate aminotransferase， gamma-glutamyl transpeptidase， alkaline phosphatase， fibronectin， triglycerides， high-density lipoprotein cholesterol， total triiodothyronine （TT3）， Homeostasis Model Assessment of Insulin Resistance （HOMA-IR）， and NFS （all P<0.05）. Compared with the non-NAFLD group， the NAFLD group had a significantly higher mRNA expression level of miR-128-3p in peripheral blood （t=-8.765， P<0.001） and significant reductions in the mRNA and proteins expression levels of SIRT1 and AMPK （P<0.001）. There were significant differences between the progressive liver fibrosis group and the non-progressive liver fibrosis group in age， ALT， free triiodothyronine， TT3， superoxide dismutase， and miR-128-3p （all P<0.05）. The logistic regression analysis showed that miR-128-3p was an independent risk factor for the development of NAFLD （odds ratio ［OR］=8.221， 95% confidence interval ［CI］： 2.735 — 24.714， P<0.001） and progressive liver fibrosis （OR=1.493， 95%CI： 1.117‍ ‍—‍ ‍1.997， P=0.007）. The ROC curve analysis showed that miR-128-3p had an area under the ROC curve of 0.890 （95%CI： 0.829 — 0.950）， with an optimal cut-off value of 13.165， a sensitivity of 89.3%， and a specificity of 72.7%. ConclusionThere is an increase in the expression of miR-128-3p in peripheral blood of T2DM patients with NAFLD， while there are reductions in the expression levels of SIRT1 and AMPK， suggesting that miR-128-3p has a certain diagnostic value in identifying NAFLD and liver fibrosis in such population.