BACKGROUND: Changes in N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels may not fully translate into patient-reported health status in patients with heart failure (HF). We aimed to evaluate the correlation between NT-proBNP levels and patient-reported health status changes at one month after discharge of patients, and their associations with risk of death and rehospitalization in patients with acute HF. METHODS: We used data from the China Patient-centered Evaluative Assessment of Cardiac Events Prospective Heart Failure Study (PEACE 5p-HF Study). Patient-reported health status was measured by the 12-item Kansas City Cardiomyopathy Questionnaire (KCCQ-12). Patients who were hospitalized for HF and completed the KCCQ-12 and NT-proBNP tests before and one month after discharge were eligible in our study. We stratified patients into different groups based on NT-proBNP levels (i.e., improved, stable, and deteriorated) and KCCQ-12 scores (i.e., not deteriorated and deteriorated). We also examined the associations of the joint NT-proBNP and KCCQ-12 change with the risk of one-year and four-year clinical outcomes. RESULTS: A total of 2461 patients were included in the analysis. The mean age was 64.06 ± 13.51 years, and 36.37% (895/2461) of the study population were female. Among patients with improved NT-proBNP levels, 115 (10.95%) patients had deteriorated KCCQ-12 scores. The correlation between the change in the KCCQ-12 score and NT-proBNP level was weak ( r2 = 0.002, P = 0.013). Stratification by changes in the KCCQ-12 score revealed subgroups with distinctive risks, such that patients with deteriorated KCCQ-12 scores in any of the NT-proBNP change groups exhibited an increased risk of one-year all-cause death than participants with not deteriorated KCCQ-12 scores in any of the NT-proBNP change groups. Patients with improved NT-proBNP levels and deteriorated KCCQ-12 scores presented greater risks of one-year all-cause death (hazard ratio [HR]: 2.45, 95% confidence interval [CI]: 1.34-4.48) than patients with stable NT-proBNP levels and not deteriorated KCCQ-12 scores (HR [95% CI], 1.77 [1.25-2.53]). CONCLUSIONS: A discrepancy between changes in NT-proBNP levels and KCCQ-12 scores was common. The change in NT-proBNP levels was not sufficient to characterize critical aspects related to HF during one month after discharge of patients. Changes in the KCCQ-12 score exhibit complementary information to NT-proBNP levels for the prediction of clinical outcomes in patients with acute HF. REGISTRATION www.clinicaltrials.gov (No. NCT02878811).
Aged ; Female ; Humans ; Male ; Middle Aged ; Health Status ; Heart Failure/metabolism* ; Natriuretic Peptide, Brain/metabolism* ; Peptide Fragments/metabolism* ; Prospective Studies

Objective:s To investigate the risk factors for delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) in patients with acute carbon monoxide poisoning (ACOP) and to develop predictive models based on machine learning algorithms.Methods:Patients with ACOP hospitalized at the First Affiliated Hospital of Zhengzhou University from August 2019 to October 2024 were included, with the occurrence of DEACMP as the outcome measure. The dataset was randomly divided into training and validation sets at a ratio of 7:3. Lasso regression was used to select features influencing the outcome in training sets. Nine machine learning models—including Random Forest (RF), Extreme Gradient Boosting (XGBoost), and Support Vector Machine (SVM)—were constructed. Receiver operating characteristic (ROC) curves were plotted and the area under the curve (AUC) calculated for each model. Calibration curves were used to assess accuracy, and decision curve analysis (DCA) was applied to evaluate clinical utility. The SHapley Additive exPlanations (SHAP) method was employed to visualize and interpret the best-performing model.Results:A total of 264 ACOP patients were included, of whom 54 (20.5%) developed DEACMP. Lasso regression identified eight key feature variables. Based on these factors, predictive models were constructed, showing good AUC stability across the nine machine learning models in both training (0.92–0.99) and validation sets (0.85–0.91). The RF model performed best, with an AUC of 0.99 in the training set and 0.90 in the validation set; its calibration curve and DCA curve also demonstrated excellent performance. SHAP analysis of the RF model revealed the importance ranking of factors from highest to lowest as follows: Glasgow Coma Scale (GCS) score, duration of coma, age, history of coronary heart disease, CK-MB level, monocyte count, diastolic blood pressure (DBP), and drinking history.Conclusions:The RF model exhibited the highest predictive performance for DEACMP occurrence in ACOP patients. The influencing factors, ranked in order of importance from highest to lowest, are as follows: GCS score, duration of coma, age, history of coronary heart disease, CK-MB level, monocyte count, DBP, and drinking history.

Objective To investigate the dynamic characteristics of intestinal pathological development at different time points in a mouse model of colitis-associated colon cancer.Methods A colitis-cancer model was established in C57BL/6 mice using azoxymethane(AOM)combined with dextran sulfate sodium(DSS).Samples were collected at 7,10,and 14 weeks post-modeling and the spleen index,colon length,mass,and colon mass per unit length were measured.Histopathological changes in the colon were observed by hematoxylin and eosin and Masson staining.Expression levels of the cancer stem cell marker CD44 and Wnt signaling pathway genes Wnt2b,Lrp5,Axin2,and Znrf3 at different pathological stages were detected by reverse transcription quantitative real time PCR.Cancer-associated fibroblasts(FAP),CD44,the proliferation marker Ki67,and goblet cell MUC2 protein were detected by multiple immunofluorescence histochemistry(mIHC)and immunofluorescence.In addition,colon organoids were isolated from model mice at ten and fourteen weeks and cultured in vitro to observe changes in organoid morphology and marker expression.Results AOM/DSS-induced mice showed reduced,distorted,and branched colon crypt structures with a few collagen fibers at 7 weeks,and varying degrees of colon intraepithelial neoplasia,with an increased proportion of high-grade intraepithelial neoplasia over time and increased collagen fiber staining at ten and fourteen weeks.mRNA levels of CD44 and Wnt2b in the colon were significantly increased(P＜0.05)and Axin2 was decreased(P＜0.01)in model mice compared with control mice at fourteen week,and levels of Wnt2b,Lrp5,and Znrf3 were increased compared with seven-week mice(P＜0.01,P＜0.05,P＜0.01),and Axin2 was decreased(P＜0.01).mIHC staining showed increased expression of FAP and CD44 in the colon in model mice at ten and fourteen weeks,with decreased MUC2 expression.Colon organoids showed cystic dilation,especially at fourteen weeks,with more prominent expression of Ki67 and CD44.Conclusions The AOM/DSS-induced mouse model exhibited chronic colonic inflammation,low-grade intraepithelial neoplasia,and high-grade intraepithelial neoplasia at seven,ten,and fourteen weeks,respectively.The pathological microenvironment was characterized by fibroblast activation and abnormal proliferation of epithelial cells.

Objective To investigate the dynamic characteristics of intestinal pathological development at different time points in a mouse model of colitis-associated colon cancer.Methods A colitis-cancer model was established in C57BL/6 mice using azoxymethane(AOM)combined with dextran sulfate sodium(DSS).Samples were collected at 7,10,and 14 weeks post-modeling and the spleen index,colon length,mass,and colon mass per unit length were measured.Histopathological changes in the colon were observed by hematoxylin and eosin and Masson staining.Expression levels of the cancer stem cell marker CD44 and Wnt signaling pathway genes Wnt2b,Lrp5,Axin2,and Znrf3 at different pathological stages were detected by reverse transcription quantitative real time PCR.Cancer-associated fibroblasts(FAP),CD44,the proliferation marker Ki67,and goblet cell MUC2 protein were detected by multiple immunofluorescence histochemistry(mIHC)and immunofluorescence.In addition,colon organoids were isolated from model mice at ten and fourteen weeks and cultured in vitro to observe changes in organoid morphology and marker expression.Results AOM/DSS-induced mice showed reduced,distorted,and branched colon crypt structures with a few collagen fibers at 7 weeks,and varying degrees of colon intraepithelial neoplasia,with an increased proportion of high-grade intraepithelial neoplasia over time and increased collagen fiber staining at ten and fourteen weeks.mRNA levels of CD44 and Wnt2b in the colon were significantly increased(P＜0.05)and Axin2 was decreased(P＜0.01)in model mice compared with control mice at fourteen week,and levels of Wnt2b,Lrp5,and Znrf3 were increased compared with seven-week mice(P＜0.01,P＜0.05,P＜0.01),and Axin2 was decreased(P＜0.01).mIHC staining showed increased expression of FAP and CD44 in the colon in model mice at ten and fourteen weeks,with decreased MUC2 expression.Colon organoids showed cystic dilation,especially at fourteen weeks,with more prominent expression of Ki67 and CD44.Conclusions The AOM/DSS-induced mouse model exhibited chronic colonic inflammation,low-grade intraepithelial neoplasia,and high-grade intraepithelial neoplasia at seven,ten,and fourteen weeks,respectively.The pathological microenvironment was characterized by fibroblast activation and abnormal proliferation of epithelial cells.

Objective To explore the effect of ligustrazine on the learning and memory function of rats with aluminum-induced cognitive impairment and its mechanism.Methods Sixty male Wistar rats were divided into a blank control group,a model group,a low-dose ligustrazine group,a high-dose ligustrazine group,and a piracetam group using a random number table method,with 12 rats in each group.The rats in the blank control group were not subjected to any treatment;the rats in the model group,low-dose ligustrazine group,high-dose ligustrazine group,and piracetam group were first prepared with aluminum toxicity models by daily gavage of 100 mg·kg-1 AlCl3 solution.After successful modeling,the rats in the piracetam group were intragastrically administered with piracetam at a dose of 400 mg·kg-1,while rats in the low-dose and high-dose ligustrazine groups were intragastrically administered with 100 and 200 mg·kg-1 ligustrazine,respectively;the rats in the blank control group and the model group were intragastrically administered with the same volume of physiological saline.All rats in the five groups received intragas tric administration once a day for 30 consecutive days.After 30 days of intervention,the Morris water maze test was used to evaluate the learning and memory function of rats in the five groups.After completing the water maze experiment,rats in the five groups were anesthetized with 200 g·L-1 chloral hydrate,and their brain tissues were quickly removed after decapitation.Immunohistochemical staining was used to observe the expression of calcium voltage-gated channel subunit alpha 1E(CACNA1E),calmodulin(CALM),and brain-derived neurotrophic factor(BDNF)in the hippocampal CA1 region of rats in the five groups;Western blot was used to detect the relative expression levels of CACNA1E,CALM,and BDNF proteins in the hippocampal CA1 region of rats in the five groups;and real-time fluorescence quantitative polymerase chain reaction was used to detect the relative expression levels of CACNA1E,CALM,and BDNF mRNA in the hippocampal CA1 region of rats in the five groups.Results On the 1st day of the Morris water maze test,the latent periods of rats in the model group,piracetam group,low-dose ligustrazine group,and high-dose ligustrazine group were significantly higher than those in the blank control group(P＜0.05);there was no statistically significant difference in the latent periods of rats among the piracetam group,low-dose ligustrazine group,high-dose ligustrazine group,and model group(P＞0.05).On the 3rd day of the Morris water maze test,the latent periods of rats in the model group,piracetam group,low-dose ligustrazine group,and high-dose ligustrazine group were significantly higher than those in the blank control group(P＜0.05);the latent periods of rats in the piracetam group and high-dose ligustrazine group were significantly lower than those in the model group and low-dose ligustrazine group(P＜0.05);there was no statistically significant difference in the latent periods of rats between the low-dose ligustrazine group and the model group(P＞0.05).On the 5th day of the Morris water maze test,the latent periods of rats in the model group,piracetam group,low-dose ligustrazine group,and high-dose ligustrazine group were significantly higher than those in the blank control group(P＜0.05);the latent periods of rats in the piracetam group and high-dose ligustrazine group were significantly lower than those in the model group and low-dose ligustrazine group(P＜0.05);there was no statistically significant difference in the latent periods of rats between the low-dose ligustrazine group and the model group(P＞0.05).On the 3rd and 5th days of the Morris water maze test,there was no statistically significant difference in the latent periods of rats between the piracetam group and the high-dose ligustrazine group(P＞0.05).The times of rats crossing platform in the model group,piracetam group,low-dose ligustrazine group,and high-dose ligustrazine group were significantly lower than those in the blank control group,and the times of rats crossing platform in the piracetam group and high-dose ligustrazine group were significantly higher than those in the model group and low-dose ligustrazine group(P＜0.05);there was no statistically significant difference in the times of rats crossing platform between the low-dose ligustrazine group and the model group(P＞0.05);there was no statistically significant difference in the times of rats crossing platform between the piracetam group and the high-dose ligustrazine group(P＞0.05).Under the microscope,brown CACNA1E,CALM,and BDNF positive cells could be observed in the hippocampal CA1 region.The expressions of CACNA1E,CALM,and BDNF proteins in the hippocampal CA1 region of rats in the model group,piracetam group,low-dose ligustrazine group,and high-dose ligustrazine group were significantly lower than those in the blank control group,and the expressions of CACNA1E,CALM,and BDNF proteins in the hippocampal CAl region of rats in the piracetam group and high-dose ligustrazine group were significantly higher than those in the model group and low-dose ligustrazine group(P＜0.05);there was no statistically significant difference in the expressions of CACNA1E,CALM,and BDNF proteins in the hippocampal CAI region of rats between the low-dose ligustrazine group and the model group(P＞0.05);there was no statistically significant difference in the expressions of CACNA1E,CALM,and BDNF proteins in the hippocampal CA1 region of rats between the piracetam group and the high-dose ligustrazine group(P＞0.05).The relative expression levels of CACNA1E,CALM,and BDNF proteins and mRNAs in the hippocampal CA1 region of rats in the model group,piracetam group,low-dose ligustrazine group,and high-dose ligustrazine group were significantly lower than those in the blank control group(P＜0.05);the relative expression levels of CACNA1E,CALM,and BDNF proteins and mRNAs in the hippocampal CA1 region of rats in the piracetam group and high-dose ligustrazine group were significantly higher than those in the model group and low-dose ligustrazine group(P＜0.05);there was no statistically significant difference in the relative expression levels of CACNA1E,CALM,and BDNF proteins and mRNAs in the hippocampal CA1 region of rats between the low-dose ligustrazine group and the model group(P＞0.05);there was no statistically significant difference in the relative expression levels of CACNA1E,CALM,and BDNF proteins and mRNAs in the hippocampal CA1 region of rats between the piracetam group and the high-dose ligustrazine group(P＞0.05).Conclusion Ligustrazine has significant protective effects on aluminum-induced cognitive impairment in rats and can greatly enhance the learning and memory function of rats.The mechanism may be related to the up-regulation of CANA1E,CALM and BDNF expression in the brain induced by ligustrazine.

This paper provides a comprehensive analysis of the current state of intelligent ophthalmology in China, including technological advancements, academic exchange platforms, policy support, future challenges, and potential solutions. Technologically, remarkable progress have been made in various areas of intelligent ophthalmology in China, including diabetic retinopathy, fundus image analysis, and crucial aspects such as quality assessment of medical artificial intelligence products, clinical research methods, technological evaluation, and industrial standards. Researchers are constantly improving the safety and standardization of intelligent ophthalmology technology by formulating clinical application guidelines and standards. Academic exchange platforms have been established to provide extensive collaboration opportunities for professionals across diverse fields, and various academic journals serve as publication platforms for intelligent ophthalmology research. Regarding public policy, the Chinese government has not only established a supportive policy environment for the advancement of intelligent ophthalmology through various documents and regulations, but provided a legal basis and management framework. However, there are still challenges to overcome, such as technological innovation, data privacy and security, outdated regulations, and talent shortages. To tackle these issues, there is a requirement for increased technological research and development, the establishment of regulatory frameworks, talent cultivation, and greater awareness and acceptance of new technologies among patients. By comprehensively addressing these challenges, intelligent ophthalmology in China is expected to continue leading the industry's global development, bringing more innovation and convenience to the field of ophthalmic healthcare.

ObjectiveTo explore the effect of Qingre Huayu Jianpi prescription （QHJ） on colitis-associated colorectal cancer （CAC） in mice， and its related mechanism. MethodC57BL/6 mice were randomly divided into four groups including the normal， model， QHJ low-dose （QHJ-L， 10 g·kg^-1）， and QHJ high-dose （QHJ-H， 40 g·kg^-1） groups. Azoxymethane （AOM） and dextran sodium sulfate （DSS） were combined to chemically build a CAC mouse model for 14 weeks. Each drug group was given intragastrically from the 5^th week to the 14^th week， once per day. An equal volume of water was fed to the normal and model groups. The mouse survival rate， colon length， weight， and pathological alterations were assessed. The protein expressions of Wnt-3a protein signaling （Wnt3a）， β-catenin， Non-phosphor-β-catenin （Non-p-β-catenin）， and cholesterol-binding glycoproteins 133 （CD133） were detected by Western blot. The localization and expression of the cluster of differentiation （CD） 80 and CD11 antigen-like family member B （CD11b） were detected by immunohistochemistry （IHC）. The colon organoids derived from CAC mice were isolated and cultured to detect the expression of Wnt signaling pathway-related proteins. ResultThe survival rate of the CAC mice was improved by QHJ treatment and the number of colon tumors was inhibited significantly. Compared with those in the normal group， the expression levels of Wnt3a， β-catenin， Non-p-β-catenin， and CD133 in colon tissues in the model group were significantly increased （P<0.05， P<0.01）. Compared with those in the model group， the levels of Wnt3a and β-catenin in the QHJ-L group were significantly decreased （P<0.01）， and the protein levels of Wnt3a， β-catenin， Non-p-β-catenin， and CD133 in the QHJ-H group were significantly decreased （P<0.05， P<0.01）. Meanwhile， the expression level of CD11b in the model group was significantly increased compared with that in the normal group while the CD80 level was significantly decreased （P<0.05， P<0.01）. Compared with those in the model group， CD11b in QHJ-L and QHJ-H groups was significantly decreased， and CD80 was significantly increased（P<0.05， P<0.01）. The expressions of Non-p-β-catenin and CD133 in colonic organoids of CAC model mice were significantly increased， while QHJ treatment could inhibit the expressions of Non-p-β-catenin and CD133 in colonic organoids （P<0.01）. ConclusionQHJ could inhibit the inflammation-cancer development in CAC mice， the mechanism of which might be related to regulating the microenvironment and inhibiting the over-activation of Wnt signaling.

Objective: To investigate the epidemiological characteristics of hand, foot, and mouth disease (HFMD) in Haishu District, Ningbo City, Zhejiang Province from 2011 to 2022, so as to provide the basis for the formulation of HFMD prevention and control strategies. Methods: Data of HFMD in Haishu District from 2011 to 2022 were collected from Chinese Disease Prevention and Control Information System, and the epidemiological and etiological characteristics were analyzed using a descriptive epidemiological method. The trends in incidence of HFMD and prevalence of positive etiological tests were analyzed using annual percent change (APC). Results: A total of 33 334 cases of HFMD were reported in Haishu District from 2011 to 2022, with an average annual reported incidence of 279.16/105, showing no significant trend (APC=-5.492%, P>0.05). The average annual reported incidence of HFMD was lower after the enterovirus 71 vaccine was launched (from 2017 to 2022) than before (from 2011 to 2016; 219.69/105 vs. 343.70/105, P<0.05). The incidence of HFMD showed seasonal characteristics, with a peak from May to July. There were 19 720 male and 13 614 female cases, with a male-to-female ratio of 1.45∶1. The age of the HFMD cases ranged from 27 days to 63 years old, and the children aged 5 years and below were predominant (30 657 cases, 91.97%). A total of 1 976 specimens of HFMD cases were collected from 2011 to 2022, and 1 509 enterovirus positive specimens were detected, with a positive rate of 76.37%. The positive rates of enterovirus 71 decreased (APC=-32.599%, P<0.05), the positive rates of coxsackievirus A16 increased (APC=9.226%, P<0.05), while the positive rates of other enteroviruses showed no significant change (APC=0.808%, P>0.05). Conclusions The average annual reported incidence of HFMD in Haishu District from 2011 to 2022 decreased after the enterovirus 71 vaccine was launched, with a peak in spring and summer. Children aged 5 years and below were the high-incidence population, and coxsackievirus A16 was the main serotype.

Objective:To analyze the epidemiological characteristics of reinfection of 2019-nCoV and influencing factors, and provide evidence for effective prevention and control of COVID-19 epidemic.Methods:The incidence data of COVID-19 in Ningbo from January 1, 2020 to November 30, 2022 were collected from the infectious disease surveillance system of Chinese information system for disease control and prevention. The incidence of reinfection of 2019-nCoV was investigated by using questionnaire. logistic regression analysis was used to analyze the influences of gender, age, time interval from the first infection, history of underlying disease, 2019-nCoV vaccination dose and disease severity on the reinfection.Results:A total of 897 previous 2019-nCoV infection cases were investigated, of which 115 experienced the reinfection of 2019-nCoV, the reinfection rate was 12.82%. The interval between the two infections M( Q1, Q3) was 1 052 (504, 1 056) days. Univariate analysis showed that age, 2019-nCoV vaccination dose, history of underlying disease, type of 2019-nCoV variant causing the first infection, time interval from the first infection and severity of the first infection were associated with the reinfection rate (all P<0.05). Multivariate logistic regression analysis showed that the risk for reinfection in age group 30- years was higher than that in age group ≥60 years ( OR=2.10, 95% CI: 1.11-3.97). No reinfection occurred in those with time interval from the first infection of <6 months, and the risk for reinfection was higher in those with the time interval of ≥12 months than in those with the time interval of 6- months ( OR=6.68, 95% CI: 3.46-12.90). The risk for reinfection was higher in the common or mild cases than in the asymptomatic cases ( OR=2.64, 95% CI: 1.18-5.88; OR=2.79, 95% CI: 1.27-6.11). Conclusion:The time interval from the first infection was an important influencing factor for the reinfection of 2019-nCoV, and the probability of the reinfection within 6 months was low.

ObjectiveTo explore the intervention effect and mechanism of Buzhong Yiqiwan （BZYQ） on colitis mice. MethodSixty-four C57BL/6 mice were randomly divided into 2 weeks blank group， 2 weeks model group， 2 weeks high-dose BZYQ （12 g·kg^-1） group， 2 weeks low-dose BZYQ （6 g·kg^-1） group， 4 weeks blank group， 4 weeks model group， 4 weeks high-dose BZYQ （12 g·kg^-1） group， and 4 weeks low-dose BZYQ （6 g·kg^-1） group. The colitis model was induced in mice by feeding 3% dextran sodium sulfate （DSS） for 7 days. The mice received BZYQ （12 and 6 g·kg^-1） by gavage on the 8^th day after modeling， once per day， and sacrificed on the 2^nd and 4^th weeks， correspondingly. The colon length and weight of mice in each group were measured. Hematoxylin-eosin （HE） staining was used for pathological observation and colonic mucosal inflammation was scored. The mRNA and protein expression of NOD-like receptor thermoprotein domain 3 （NLRP3）， apoptosis-associated speck-like protein containing a CARD （ASC）， and cysteinyl aspartate-specific protease-1 （Caspase-1） was detected by real-time quantitative polymerase chain reaction （Real-time PCR） and Western blot， respectively. Enzyme-linked immunosorbent assay （ELISA） was used to detect the content of inflammatory cytokines， such as interleukin （IL）-1β， IL-18， and IL-33 in colonic tissues. ResultCompared with the 2 weeks blank group， the 2 weeks model group showed shortened colon length， increased colon weight （P<0.05）， loss of epithelial cells， destruction of gland structure， infiltration of a large number of inflammatory cells in mucosa and submucosa， local crypt abscess， and increase in mucosal inflammation score （P<0.01） as revealed by light microscopy， elevated levels of IL-1β， IL-18， and IL-33 in colonic tissues （P<0.05）， and increased mRNA and protein expression of NLRP3， ASC， and Caspase-1 （P<0.05）. The intervention of BZYQ （12 g·kg^-1） restored colon length， alleviated mucosal injury （P<0.05）， down-regulated the content of IL-18 （P<0.05）， reduced the mRNA expression of NLRP3 and ASC as well as the protein expression of ASC and Caspase-1 compared with the conditions in the 2 weeks model group. Compared with the 4 weeks blank group， the 4 weeks model group showed decreased colon length， increased colon weight （P<0.05）， decreased glands in the mucosal layer， expansion of glandular cavity， atrophy of crypt， local connective tissue hyperplasia and lymphocyte infiltration， increased inflammation score （P<0.01） as revealed by the light microscopy， increased expression of IL-1β， IL-18， and IL-33 （P<0.05）， and elevated mRNA and expression of NLRP3 inflammasome complex （P<0.05）. Compared with the conditions in the 4 weeks model group， the intervention of BZYQ （12 and 6 g·kg^-1） could improve colon length and weight （P<0.05）， and the intervention of BZYQ （12 g·kg^-1） could also improve the inflammation score of the colon （P<0.05）. Different from the acute stage， the intervention of BZYQ （12 and 6 g·kg^-1） increased the content of IL-33 in the intestinal mucosa and up-regulated the mRNA and protein expression of NLRP3 inflammasome complexes ASC and Caspase-1 （P<0.05）. ConclusionBZYQ can relieve the injury of colitis induced by DSS in mice. The mechanism is related to the regulation of intestinal immune response mediated by NLRP3 inflammasome， and it has different regulatory effects in acute and chronic inflammation stages.