Bronchial asthma （abbreviated as asthma） is one of the common inflammatory diseases in the chronic airway of the respiratory system. Recurrent wheezing，shortness of breath，chest tightness， and cough are the main symptoms，which are easy to repeat，protracted and difficult to cure，and seriously affect the patients' life quality. The Janus kinases （JAK）/signal transducers and activators of transcription （STAT） signaling pathway is involved in the regulation of cellular inflammatory response，oxidative stress，apoptosis， and other biological processes. It plays a key role in the occurrence and development of asthma. Traditional Chinese medicine intervenes in asthma based on the JAK/STAT signaling pathway in multiple stages and targets. The specific mechanism is related to inhibiting airway inflammation and anti-oxidative stress，alleviating airway remodeling，affecting airway mucus hypersecretion，inhibiting high airway response， and regulating immune response，which demonstrates the characteristics and advantages of traditional Chinese medicine in treating asthma. Based on this，by referring to relevant literature，this paper systematically sorted out the JAK/STAT signaling pathway and its action mechanism in the occurrence and development of asthma. It also systematically summarized the efficacy and specific mechanism of monomers， compounds， and compound formulas of traditional Chinese medicine， as well as the external treatment methods by regulating the JAK/STAT signaling pathway to intervene in asthma. It aims to effectively prevent and control the occurrence and development of asthma in clinic， providing a reference for the methods of prevention and treatment of asthma with traditional Chinese medicine.

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.

Bronchial asthma （abbreviated as asthma） is one of the common chronic airway inflammatory diseases in the respiratory system， which is difficult to cure. Airway mucus hypersecretion （AMH） is an important factor leading to acute asthma attacks. Traditional Chinese medicine （TCM） possesses therapeutic advantages characterized by multiple pathways， multiple targets， and multiple links， and its mechanism of action in intervening in AMH has gradually drawn attention. TCM can effectively alleviate the symptoms of patients by intervening in asthma through methods such as eliminating phlegm and eliminating fluid retention. This review finds that the pathogenesis of asthma-associated AMH is correlated with decreased mucociliary clearance function and enhanced mucus secretion function； single TCM （such as Platycodon grandiflorum）， effective components of TCM （such as pinellia polysaccharides）， and compound prescriptions （mainly heat-clearing and phlegm-resolving prescriptions， etc.） can improve asthma-associated AMH by regulating the PI3K/Akt and JAK/STAT signaling pathways， inhibiting airway inflammatory responses， oxidative stress， and recovering the water-salt ratio of the mucus layer itself.

Objective:To investigate the effect of polystyrene microplastics(PS-MPs)combined with high-fat treatment on vascular endothelial cells.Methods:Human umbilical vein endothelial cells(HUVECs)were cultured in the DMEM medium containing 5%fe-tal bovine serum.HUVECs were treated with conventional culture,high-fat treatment,and PS-MPs combined with high-fat treatment.The experiment was conducted in the three groups of control group,high-fat treatment group and PS-MPs+high-fat treatment group.CCK-8 assay was used to measure cell viability,F-actin staining was used to observe cell morphological changes,and flow cytometry,scratch assay,and tube formation assay were used to measure the apoptosis,migration,and tube-forming ability of cells.Results:After HUVECs were exposed to the high-fat environment,there was a significant reduction in cell viability,shrinkage of cells,a signifi-cant increase in cell apoptosis,and significant reductions in cell migration and tube-forming ability.Compared with the high-fat treat-ment group,there were no significant changes in cell viability,cell morphology,cell apoptosis,and cell migration ability after PS-MPs combined with high-fat treatment,but the tube-forming ability of cells was further impaired.Conclusion:High-fat treatment will affect cell viability,change cell morphology,and damage vascular endothelial cell function,and PS-MPs combined with high-fat treat-ment can aggravate the damage of vascular endothelial cell function.

Objective:To investigate the role of alkylation repair homolog 5(ALKBH5)-mediated N6-methyladenosine(m6A)modifi-cation in endometrial decidualization.Methods:The mouse models of pregnancy and pseudopregnancy were established,and quantita-tive real-time PCR and Western blot were used to measure the expression pattern of ALKBH5 in the endometrium.The mouse and cell models of artificially induced decidualization were established,and quantitative real-time PCR,Western blot,and immunohistochemis-try were used to measure the expression levels of decidualization-related markers.The EpiQuik m6A RNA methylation quantification kit was used to measure the level of m6A.The mouse and cell models of artificially induced decidualization with interference of ALKBH5 expression were established,and quantitative real-time PCR,Western blot,and immunohistochemistry were used to measure the expression levels of decidualization-related markers,cell proliferation marker molecules,and apoptosis molecules.Flow cytometry was used to measure cell apoptosis rate.Results:In the mouse model of pregnancy,the expression level of ALKBH5 at the uterine em-bryo implantation site was significantly higher than that adjacent to the implantation site,and in the mouse and cell models of artifi-cially induced decidualization,compared with the control group,the induction group had a significant increase in the expression level of ALKBH5 and a significant reduction in the level of m6A.Inhibiting the expression of ALKBH5 led to an increase in the level of m6A,which in turn inhibited the proliferation of stromal cells,induced cell apoptosis,and ultimately impaired the normal process of en-dometrial decidualization.Conclusion:ALKBH5 deficiency leads to an increase in the level of m6A and decidualization injury in the en-dometrium,which lays a foundation for the research on m6A modifi-cation in decidualization.

OBJECTIVE To evaluate the comprehensive quality of Houttuynia cordata from different producing areas. METHODS Using total flavonoids， water-soluble extract， moisture， total ash and acid-insoluble ash as indicators， the entropy weight method was used to objectively weigh each indicator， and the relative correlation degree （r）i calculated by grey correlation method was used as a measure to comprehensively evaluate the quality of H. cordata. RESULTS The weights of total flavonoids， total ash， moisture， acid-insoluble ash， and water-soluble extract were 0.295 5， 0.227 3， 0.188 7， 0.145 1， and 0.143 4， respectively. The weights of total flavonoids and total ash were relatively large. The ri of 30 batches of H. cordata ranged from 0.233 2 to 0.673 9； the average ri of samples from Quanzhou County and Ziyuan County of Guangxi Zhuang Autonomous Region were the highest， which were 0.638 3 and 0.598 7， respectively， followed by samples from Lingchuan County of Guangxi Zhuang Autonomous Region （0.556 1） and Jianshui County of Yunnan Province （0.452 8）. The quality of medicinal materials produced in the above producing areas was generally good and stable. CONCLUSIONS Entropy weight method combined with the grey correlation method can be used to comprehensively evaluate the quality of H. cordata. The overall quality of H. cordata produced in Quanzhou County of Guangxi Zhuang Autonomous Region is the best.

BACKGROUND/OBJECTIVES: Sanghuangporus sanghuang (SS) has various medicinal effects, including anti-inflammation and anticancer activities. Despite the extensive research on SS, its molecular mechanisms of action on lung cancer are unclear. This study examined the impact of an SS alcohol extract (SAE) on lung cancer using in vitro and in vivo models.MATERIALS/METHODS: Different concentrations of SAE were used to culture lung cancer cells (A549 and H1650). A cell counting kit-8 assay was used to detect the survival ability of A549 and H1650 cells. A scratch assay and transwell cell invasion assay were used to detect the migration rate and invasive ability of SAE. Western blot analysis was used to detect the expression of B-cell lymphoma-2 (Bcl-2), Bcl2-associated X (Bax), cyclin D1, cyclin-dependent kinases 4 (CDK4), signal transducer and activator of transcription 3 (STAT3), and phosphorylated STAT3 (p-STAT3). Lung cancer xenograft mice were used to detect the inhibiting ability of SAE in vivo.Hematoxylin and eosin staining and immunohistochemistry were used to detect the effect of SAE on the structural changes to the tumor and the expression of Bcl-2, Bax, cyclin D1, CDK4, STAT3, and p-STAT3 in lung cancer xenograft mice. RESULTS: SAE could inhibit lung cancer proliferation significantly in vitro and in vivo without cytotoxicity. SAE suppressed the viability, migration, and invasion of lung cancer cells in a dose and time-dependent manner. The SAE treatment significantly decreased the proapoptotic Bcl-2/Bax ratio and the expression of pro-proliferative proteins Cyclin D1 and CDK4 in vitro and in vivo. Furthermore, SAE also inhibited STAT3 expression. CONCLUSIONS SAE reduced the cell viability and suppressed cell migration and invasion in human lung cancer cells. Moreover, SAE also exhibited anti-proliferation effects in vivo. Therefore, SAE may have benefits in cancer therapy.

BACKGROUND: Dysfunction of the gap junction channel protein connexin 43 (Cx43) contributes to myocardial ischemia/reperfusion (I/R)-induced ventricular arrhythmias. Cx43 can be regulated by small ubiquitin-like modifier (SUMO) modification. Protein inhibitor of activated STAT Y (PIASy) is an E3 SUMO ligase for its target proteins. However, whether Cx43 is a target protein of PIASy and whether Cx43 SUMOylation plays a role in I/R-induced arrhythmias are largely unknown. METHODS: Male Sprague-Dawley rats were infected with PIASy short hairpin ribonucleic acid (shRNA) using recombinant adeno-associated virus subtype 9 (rAAV9). Two weeks later, the rats were subjected to 45 min of left coronary artery occlusion followed by 2 h reperfusion. Electrocardiogram was recorded to assess arrhythmias. Rat ventricular tissues were collected for molecular biological measurements. RESULTS: Following 45 min of ischemia, QRS duration and QTc intervals statistically significantly increased, but these values decreased after transfecting PIASy shRNA. PIASy downregulation ameliorated ventricular arrhythmias induced by myocardial I/R, as evidenced by the decreased incidence of ventricular tachycardia and ventricular fibrillation, and reduced arrythmia score. In addition, myocardial I/R statistically significantly induced PIASy expression and Cx43 SUMOylation, accompanied by reduced Cx43 phosphorylation and plakophilin 2 (PKP2) expression. Moreover, PIASy downregulation remarkably reduced Cx43 SUMOylation, accompanied by increased Cx43 phosphorylation and PKP2 expression after I/R. CONCLUSION PIASy downregulation inhibited Cx43 SUMOylation and increased PKP2 expression, thereby improving ventricular arrhythmias in ischemic/reperfused rats heart.
Rats ; Male ; Animals ; Myocardial Reperfusion Injury/metabolism* ; Connexin 43/genetics* ; Sumoylation ; Down-Regulation ; Rats, Sprague-Dawley ; Arrhythmias, Cardiac/drug therapy* ; Myocardial Ischemia/metabolism* ; RNA, Small Interfering/metabolism*

ObjectiveTo explore the dynamic evolution law of syndrome elements in different stages of chronic obstructive pulmonary disease （COPD）. MethodThe clinical questionnaire of COPD was formulated，and the clinical data of 303 patients with COPD in the acute exacerbation stage，risk window stage，and stable stage in the First Affiliated Hospital of Henan University of Chinese Medicine from June 2019 to December 2020 were dynamically collected. The Clinical Investigation and Research Database on the Evolution of Syndrome Elements of COPD was established，with syndrome elements as nodes and complex relationships between syndrome elements and syndrome elements in different stages as edges. With the help of Pycharm （JetBrains PyCharm Edition 2018.2.3） development tool，python programming was used to preprocess the data and perform complex network modeling. The complex network of different stages of COPD was constructed to analyze the evolution law of syndrome factors in different stages. ResultA total of 303 patients with COPD were included and finished. Eleven syndrome elements were extracted in the acute exacerbation stage，10 syndrome elements were extracted in the risk window stage，and 8 syndrome elements were extracted in the stable stage. According to the complex network centrality and edge weight of disease syndrome elements，it was found that the core nodes of disease syndrome elements in the network from the acute exacerbation stage to the stable stage were phlegm，heat，and Qi deficiency，Qi deficiency，phlegm，and dampness，and Qi deficiency，Yin deficiency，and blood stasis. ConclusionFrom the acute exacerbation stage to the stable stage，the disease syndrome elements change from excess to deficiency，and phlegm heat gradually changes into phlegm dampness，and gradually weakens or disappears. Qi deficiency runs through the whole process of the disease and turns into both qi and yin deficiency with blood stasis.

OBJECTIVE：To establish the method for determining protein binding rate of dipeptidyl peptidase- 4 inhibitor LGT- 6 in different species of plasma ，and to compare their difference. METHODS ：By equilibrium dialysis ，LGT-6（3，30，300，3 000 nmol/L）was equilibrated in rat ，monkey and human plasma （i. e. internal dialysis solution ）for 48 h，using phosphate buffer as the external dialysis solution. The concentration of LGT- 6 in internal and external dialysis solution was determined by UPLC-MS/MS using tolbutamide as internal standard ，and the plasma protein binding rate was calculated. The determination was performed on ACQUITY UPLC HSS T 3 column with water （containing 0.01％ formic acid ）-acetonitrile（containing 0.01％ formic acid ）as mobile phase at the flow rate of 0.6 mL/min. The column temperature was 40 ℃，and the sample size was 2 μL. The ion source was electrospray ion source ，and the multiple ion monitoring mode was used to carry out positive ionization scanning. The ion pairs for quantitative analysis were m/z 487.0→434.3（LGT-6），m/z 271.1→172.0（internal standard ），respectively. RESULTS ：At the concentrations of 3，30，300，and 3 000 nmol/L，the protein binding rates of LGT- 6 in rat plasma were （96.25±0.97）％，（84.16± 1.24）％，（78.25±0.61）％，（66.63±0.95）％；the protein protein binding rates in monkey plasma were （98.54±0.58）％，（87.27± 1.01）％，（79.35±0.86）％，（66.69±0.54）％；the protein binding rates in human plasma were （99.40±1.03）％，（84.48± 1.15）％，（77.62±0.77）％，（66.93±0.48）％. At the same concentration ，the protein binding rates of LGT- 6 in rat ，monkey and human plasma had no significant difference （P＞0.05）. In the same species of plasma ，there were significant differences in the plasma protein binding rates of different concentration of LGT-6 among those groups （P＜0.05），and it decreased with 才〔2016〕4015） the increase of drug concentration. CONCLUSIONS ： The method for the determination of plasma protein binding rate of LGT-6 is successfully established. The data revealed that the protein binding rate of LGT- 6 is concentration-dependent ， there was no obvious spec ies difference on protein binding rates of LGT- 6 in rat ，monkey and human plasma under the same concentration.