ObjectiveExploring the formula rules of commonly used traditional Chinese medicines（TCMs） for epidemic treatment from the Qin and Han dynasties to the Qing dynasty through data mining， providing reference for the prevention and control of contemporary epidemics. MethodsThe articles on epidemic treatment in the electronic database of Chinese Medical Code V5.0 were systematically searched， and the contents such as source， dynasty， author， diagnosis， formula name， therapeutic method and efficacy， and composition of medicines from each article that met the inclusion criteria were extracted. Then， an Excel standardized database was established， and Python programs were used for data mining to summarize the frequency of commonly used medicines and perform hierarchical cluster analysis， Pearson correlation analysis， and association rule analysis. ResultsA total of 1 595 formulas were included， involving 558 TCMs. The efficacy of these medicines could be classified into two categories， namely， expeling pathogenic factors and reinforcing healthy Qi. According to the frequency deconstruction analysis， high-frequency medicines were mainly detoxification， Fu-organ dredging， aromatization and promoting blood circulation， followed by the medicines with the effect of treating the lungs， such as clearing the lungs and resolving phlegm， clearing heat and purging the lungs， relieving cough and asthma， and purging the lungs and relieving asthma. And the proportions of acrid-warm herbs and acrid-cold herbs varied in different periods. Hierarchical clustering and correlation analysis both suggested TCMs for expeling pathogenic factors and reinforcing healthy Qi often formed stable combinations with high association degrees. Association rule analysis showed that the core acrid-warm herb was mainly Ephedrae Herba， and the core acrid-cold herb was mainly Forsythiae Fructus， resulting in the core formulas of Maxing Shigantang and Yinqiaosan. ConclusionThroughout history， the prevention and control of epidemics have been based on the principle of "preserving healthy Qi and avoiding toxic Qi"， focusing on the treatment of the causes and characteristics of epidemics through detoxification， Fu-organ dredging， and aromatization， emphasizing the use of Rhei Radix et Rhizoma and other herbs to dredge Fu-organ， eliminate toxins and pathogens， and playing the role of actively intervene with symptomatic medication. And based on the external manifestations of the body's struggle between evil and righteousness， diagnose and treatment according to syndrome differentiation was performed.

ObjectiveExploring the formula rules of commonly used traditional Chinese medicines（TCMs） for epidemic treatment from the Qin and Han dynasties to the Qing dynasty through data mining， providing reference for the prevention and control of contemporary epidemics. MethodsThe articles on epidemic treatment in the electronic database of Chinese Medical Code V5.0 were systematically searched， and the contents such as source， dynasty， author， diagnosis， formula name， therapeutic method and efficacy， and composition of medicines from each article that met the inclusion criteria were extracted. Then， an Excel standardized database was established， and Python programs were used for data mining to summarize the frequency of commonly used medicines and perform hierarchical cluster analysis， Pearson correlation analysis， and association rule analysis. ResultsA total of 1 595 formulas were included， involving 558 TCMs. The efficacy of these medicines could be classified into two categories， namely， expeling pathogenic factors and reinforcing healthy Qi. According to the frequency deconstruction analysis， high-frequency medicines were mainly detoxification， Fu-organ dredging， aromatization and promoting blood circulation， followed by the medicines with the effect of treating the lungs， such as clearing the lungs and resolving phlegm， clearing heat and purging the lungs， relieving cough and asthma， and purging the lungs and relieving asthma. And the proportions of acrid-warm herbs and acrid-cold herbs varied in different periods. Hierarchical clustering and correlation analysis both suggested TCMs for expeling pathogenic factors and reinforcing healthy Qi often formed stable combinations with high association degrees. Association rule analysis showed that the core acrid-warm herb was mainly Ephedrae Herba， and the core acrid-cold herb was mainly Forsythiae Fructus， resulting in the core formulas of Maxing Shigantang and Yinqiaosan. ConclusionThroughout history， the prevention and control of epidemics have been based on the principle of "preserving healthy Qi and avoiding toxic Qi"， focusing on the treatment of the causes and characteristics of epidemics through detoxification， Fu-organ dredging， and aromatization， emphasizing the use of Rhei Radix et Rhizoma and other herbs to dredge Fu-organ， eliminate toxins and pathogens， and playing the role of actively intervene with symptomatic medication. And based on the external manifestations of the body's struggle between evil and righteousness， diagnose and treatment according to syndrome differentiation was performed.

Chronic obstructive pulmonary disease （COPD） is a common disease with a high incidence and mortality rate in the world. It is characterized by chronic inflammation and structural obstruction and is not completely reversible which will lead to shortness of breath caused by air retention and physical exertion. Traditional Chinese medicine proposes the concept of "lung collaterals"， which refers to the collateral vessels scattered throughout the lungs and lung system. The lung collaterals include the pulse collaterals and Qi collaterals. The blood circulation in the pulse collaterals belongs to Yin， distributed internally along the way. The Qi circulation in the Qi collateral belongs to Yang and is distributed externally. In western medicine， the pulse collaterals have an identity with large， medium， and small blood vessels， microvessels， and especially microcirculation. The Qi collateral encompasses systems such as the nervous， endocrine， and immune system. Pulmonary microvascular endothelial cells （HPMECs） are an important component of the pulmonary microvascular endothelium. Recent studies have found that HPMECs are the main damaged cells in the pathogenesis of COPD， mediating the occurrence and development of COPD. Traditional Chinese medicine can regulate HPMECs to treat COPD through multiple components， targets， and pathways， and has the advantage of reducing western medicine resistance and many side effects. Based on the "lung collateral theory"， this paper focused on HPMECs， and elaborated on the new connotation of traditional Chinese medicine in protecting HPMECs to treat COPD， aiming to provide new insights for the clinical treatment of COPD by protecting HPMECs.

Chronic obstructive pulmonary disease （COPD） is a common disease with a high incidence and mortality rate in the world. It is characterized by chronic inflammation and structural obstruction and is not completely reversible which will lead to shortness of breath caused by air retention and physical exertion. Traditional Chinese medicine proposes the concept of "lung collaterals"， which refers to the collateral vessels scattered throughout the lungs and lung system. The lung collaterals include the pulse collaterals and Qi collaterals. The blood circulation in the pulse collaterals belongs to Yin， distributed internally along the way. The Qi circulation in the Qi collateral belongs to Yang and is distributed externally. In western medicine， the pulse collaterals have an identity with large， medium， and small blood vessels， microvessels， and especially microcirculation. The Qi collateral encompasses systems such as the nervous， endocrine， and immune system. Pulmonary microvascular endothelial cells （HPMECs） are an important component of the pulmonary microvascular endothelium. Recent studies have found that HPMECs are the main damaged cells in the pathogenesis of COPD， mediating the occurrence and development of COPD. Traditional Chinese medicine can regulate HPMECs to treat COPD through multiple components， targets， and pathways， and has the advantage of reducing western medicine resistance and many side effects. Based on the "lung collateral theory"， this paper focused on HPMECs， and elaborated on the new connotation of traditional Chinese medicine in protecting HPMECs to treat COPD， aiming to provide new insights for the clinical treatment of COPD by protecting HPMECs.

Chronic obstructive pulmonary disease(COPD)is a common disease with a high global incidence and mortality rate.It is charac-terized by chronic inflammation and structural airway obstruction that is not fully reversible,leading to shortness of breath caused by air trapping and increased physical exertion.Over the past few decades,the incidence of COPD has continued to rise.Although commonly used therapeutic agents,such as glucocorticoids and bronchodilators,have demonstrated significant symptomatic relief,they primarily target symptoms rather than halting disease progression.Therefore,further research is needed to better understand the underlying mechanisms of COPD and to develop novel therapeutic strategies for its prevention and management.Early studies on the pathogenesis of COPD primarily focused on airway epithelial cell injury,while relatively less attention was given to pulmonary vascular endothelial cells(PVECs).However,recent evidence indicates that COPD is not only an airway and systemic inflammatory disorder but also a vascular disease,with PVECs playing a critical role in its pathogenesis.PVECs are among the main cellular targets damaged in COPD and are involved in mediating its initiation and progression.In this review,we summarize emerging evidence that highlights the close association between PVEC injury and COPD pathogenesis.We also explore the roles and mechanisms of various therapeutic interventions targeting PVECs,including chemical agents and traditional Chinese medicine,in the treatment of COPD.

Chronic obstructive pulmonary disease (COPD) is a common disease with a high global incidence and mortality rate. It is characterized by chronic inflammation and structural airway obstruction that is not fully reversible, leading to shortness of breath caused by air trapping and increased physical exertion. Over the past few decades, the incidence of COPD has continued to rise. Although commonly used therapeutic agents, such as glucocorticoids and bronchodilators, have demonstrated significant symptomatic relief, they primarily target symptoms rather than halting disease progression. Therefore, further research is needed to better understand the underlying mechanisms of COPD and to develop novel therapeutic strategies for its prevention and management. Early studies on the pathogenesis of COPD primarily focused on airway epithelial cell injury, while relatively less attention was given to pulmonary vascular endothelial cells (PVECs). However, recent evidence indicates that COPD is not only an airway and systemic inflammatory disorder but also a vascular disease, with PVECs playing a critical role in its pathogenesis. PVECs are among the main cellular targets damaged in COPD and are involved in mediating its initiation and progression. In this review, we summarize emerging evidence that highlights the close association between PVEC injury and COPD pathogenesis. We also explore the roles and mechanisms of various therapeutic interventions targeting PVECs, including chemical agents and traditional Chinese medicine, in the treatment of COPD.

Chronic obstructive pulmonary disease(COPD)is a common disease with a high global incidence and mortality rate.It is charac-terized by chronic inflammation and structural airway obstruction that is not fully reversible,leading to shortness of breath caused by air trapping and increased physical exertion.Over the past few decades,the incidence of COPD has continued to rise.Although commonly used therapeutic agents,such as glucocorticoids and bronchodilators,have demonstrated significant symptomatic relief,they primarily target symptoms rather than halting disease progression.Therefore,further research is needed to better understand the underlying mechanisms of COPD and to develop novel therapeutic strategies for its prevention and management.Early studies on the pathogenesis of COPD primarily focused on airway epithelial cell injury,while relatively less attention was given to pulmonary vascular endothelial cells(PVECs).However,recent evidence indicates that COPD is not only an airway and systemic inflammatory disorder but also a vascular disease,with PVECs playing a critical role in its pathogenesis.PVECs are among the main cellular targets damaged in COPD and are involved in mediating its initiation and progression.In this review,we summarize emerging evidence that highlights the close association between PVEC injury and COPD pathogenesis.We also explore the roles and mechanisms of various therapeutic interventions targeting PVECs,including chemical agents and traditional Chinese medicine,in the treatment of COPD.

ObjectiveTo investigate the effect and mechanism of ginsenoside Rg₁ （G-Rg₁） combined with hirudin in treating myocardial fibrosis in the mouse model of acute myocardial infarction （AMI）. MethodSeventy-five C57BL/6N mice were randomized into sham， model， G-Rg₁ （20 mg·kg^-1）， hirudin （20 mg·kg^-1）， and G-Rg₁ （20 mg·kg^-1） + hirudin （20 mg·kg^-1） groups. The mouse model of AMI was established by ligation of the anterior descending branch of the left coronary artery and continued gavage for 4 weeks. The success of the modeling was judged by ECG changes of mice before and after ligation. The heart weight index， echocardiography， myocardial fibrosis， type Ⅰ collagen α1（COL1A1）， platelet-endothelial cell adhesion molecule-1 （PECAM-1/CD31）， α-smooth muscle actin （α-SMA）， intercellular adhesion molecule-1 （ICAM-1）， and vascular cell adhesion molecule-1 （VCAM-1） were measured before and after treatment. ResultAfter ligation of the anterior descending branch of the left coronary artery， the R wave and T wave merged into a tall tented wave， and the ST segment presented a "damaged" change， indicating that the model was successfully prepared. Compared with the sham group， the model group showed dull and dry hair， slow movement， increased heart weight index （P<0.01）， decreased left ventricular ejection fraction （EF） and left ventricular shortening fraction （FS） （P<0.01）， increased left ventricular end-diastolic diameter （LVEDd） and left ventricular end-systolic diameter （LVESd） （P<0.01）， disarranged myocardial fibers， collagen fiber hyperplasia （P<0.01）， increased expression of COL1A1 （P<0.01）， upregulated protein levels of ICAM-1 and VCAM-1 （P<0.01）， downregulated CD31 expression， and upregulated α-SMA expression （P<0.01）. Compared with the model group， the treatment groups recovered the above indexes in different degrees （P<0.05， P<0.01）， and the combined group had better effect （P<0.05）. ConclusionG-Rg₁ combined with hirudin can ameliorate myocardial fibrosis after AMI by inhibiting the expression of adhesion molecular protein in the heart tissue， reducing the adhesion of inflammatory cells， alleviating cardiac inflammation， and inhibiting cardiac endothelial-to-mesenchymal transition.

Objective:Exploring the role and mechanism of gremlin-1 in lipotoxicity-mediated pancreatic β-cell dysfunction.Methods:The model of lipid toxicity-mediated pancreatic β-cell dysfunction was constructed using palmitic acid(PA) to treat mouse pancreatic β-cells(MIN6). Initially, to clarify the effects of lipotoxicity on islet β-cells, the cellular lipid deposition and changes in the levels of insulin caused by PA were detected. The effects of PA on gremlin-1 expression and its downstream signaling pathway BMPs/Smads were further investigated using qPCR and Western Blot assay. Subsequently, recombinant mouse gremlin-1 protein and BMP signaling pathway inhibitor LDN193189 were used to intervene the cells to explore the effects of gremlin-1 and its downstream signaling pathway BMPs/Smads on pancreatic islet β-cells.Results:PA could reduce pancreatic β-cell viability and insulin secretion capacity( P<0.05). Meanwhile, PA inhibited the expression and secretion of cell gremlin-1 and upregulated BMP-4 and its downstream Smad-1 and Smad-5( P<0.05). Intervention of cells with recombinant mouse gremlin-1 protein resulted in a significant elevation of insulin secretion and a concomitant decrease in the expression of key molecules in the BMP4/Smads signaling pathway( P<0.05). And inhibition of the BMP4/Smads signaling pathway ameliorated PA-induced pancreatic β-cell dysfunction. Conclusion:Gremlin-1 is involved in the regulation of lipotoxicity-mediated pancreatic islet β-cell dysfunction, and this effect may be associated with activation of BMP4/Smads signaling pathway.

Objective:To investigate the association of skeletal muscle fat index(SMFI) with insulin resistance and type 2 diabetes mellitus.Methods:This retrospective study included 1 100 patients from Department of Geriatric, Renji Hospital, Shanghai Jiao Tong University School of Medicine from October 2020 to October 2023. The SMFI measured by chest computed tomography(CT) is used as an indicator to evaluate the quality of skeletal muscle. Spearman and linear regression analysis were used to evaluate the association between SMFI and homoeostasis model assessment for insulin resistance(HOMA-IR). Multivariate logistic regression analysis and restricted cubic spline(RCS) were used to analyze the association of HOMA-IR with the prevalence of type 2 diabetes mellitus. Finally, interaction and stratified analyses were conducted according to age, sex, body mass index, estimated glomerular filtration rate, uric acid, skeletal muscle index(SMI), smoking, alcohol drinking, hypertension, and dyslipidemia.Results:SMFI showed a significant positive correlation with HOMA-IR( r=0.385, P<0.001). Each 1-unit increase in SMFI led to 0.009, 0.011, 0.004, 0.004, and 0.004 rise in HOMA-IR across adjusted models(all P<0.05). Then subjects were stratified into tertiles( T1, T2, and T3) according to SMFI. Logistic regression analysis revealed that the prevalence of type 2 diabetes mellitus significantly increased in T2( OR=2.37, 95% CI 1.30-4.31, P=0.005) and T3( OR=2.85, 95% CI 1.39-5.86, P=0.004) compared to T1. RCS analysis showed that the prevalence of type 2 diabetes mellitus increased with the increase of SMFI when SMFI<157.195. The results of subgroup analysis showed that female, under 60 years old, body mass index<24 kg/m 2, uric acid<420 μmol/L, low SMI, non-smoking, non-alcoholic drinking, and non-hypertensive individuals with higher SMFI were more likely to develop type 2 diabetes mellitus. Conclusions:Elevated SMFI is positively associated with insulin resistance and type 2 diabetes mellitus risk. Reducing SMFI below 157.195 may significantly lower the risk of type 2 diabetes mellitus.