Objective To investigate the influencing factors of stroke patients with hypertension and their compliance with antihypertensive drugs, and to provide targeted intervention measures for stroke prevention in hypertensive patients.  Methods Using the method of multi-stage cluster sampling, a total of 59,434 permanent residents aged 40 and above were selected from 48 monitoring sites in 9 cities of Hebei Province from December 2019 to December 2020. Unconditional logistic regression analysis was used to explore the influencing factors of stroke complicated with hypertension and the compliance of patients with antihypertensive drugs.  Results Among the 59 434 subjects, the prevalence rate of stroke was 4.33% and the prevalence rate of stroke complicated with hypertension was 82.47%. The results of univariate analysis showed that the proportion of women, rural areas, dyslipidemia, diabetes, obesity, and people with family history of stroke was higher in stroke patients with hypertension, and the difference was statistically significant (P<0.05). Multivariate logistic regression analysis showed that rural areas, dyslipidemia, diabetes, obesity, and family history of stroke significantly increased the risk of stroke, and the OR (95%CI) values were 1.29 (1.03-1.62), 1.39 (1.12-1.72), 1.58 (1.25-1.99), 1.61 (1.22-2.12) and 1.60 (1.26-2.04), respectively. Among stroke patients with hypertension, 92.71% of patients took antihypertensive drugs. It was found that women's compliance with antihypertensive drugs was good, with an OR (95%CI) value of 1.46 (1.01-2.09).  Conclusion The prevalence rate of stroke complicated with hypertension is high in people aged 40 and above in Hebei Province. Hypertensive people should lower blood lipids, control blood glucose, and lose weight as soon as possible to prevent the occurrence of stroke.

ObjectiveTo investigate the effects of modified Xiaoyaosan （JJXYS） on behavioral abnormalities and hippocampal mitochondrial quality control （MQC） in the rat model of post-myocardial infarction depression （PMD） and preliminarily explore its potential mechanism. MethodsA rat model of PMD was established by left anterior descending coronary artery ligation combined with chronic unpredictable mild stress （CUMS）. Rats were randomized into a control group， a model group， a fluoxetine （FLX， 10 mg·kg^-1） group， and low-， medium-， and high-dose JJXYS （JJXYS-L/M/H， 1.12， 2.24， 4.48 g·kg^-1， respectively） groups. Depressive-like behaviors were evaluated by body weight monitoring， sucrose preference test， open field test， and forced swimming test. Hematoxylin-eosin staining and Nissl staining were used to observe hippocampal histomorphology and neuronal changes. Enzyme-linked immunosorbent assay was conducted to determine the serum levels of 5-hydroxytryptamine （5-HT）， dopamine （DA）， interleukin-1 beta （IL-1β）， interleukin-6 （IL-6）， and tumor necrosis factor-alpha （TNF-α）. The mRNA levels of MQC-related genes including peroxisome proliferator-activated receptor-gamma coactivator-1 alpha （PGC-1α）， nuclear respiratory factor 1 （Nrf1）， and transcription factor A， mitochondrial （TFAM） in the hippocampal tissue were measured by real-time PCR. The expression of proteins related to the dynamin-related protein 1 （Drp1）/PTEN-induced putative kinase 1 （PINK1）/Parkin signaling pathway was determined by Western blot. ResultsCompared with the control group， the model group showed restricted body weight gain， aggravated depressive-like behaviors， declined serum 5-HT and DA levels， evident hippocampal neuronal damage and reduced Nissl bodies， as well as downregulated expression of MQC-related genes and proteins （P<0.05）. Compared with the model group， both FLX and JJXYS alleviated the above changes to varying degrees. Moreover， the JJXYS-M and JJXYS-H groups showed more pronounced effects， improving behavioral performance， restoring 5-HT and DA levels， alleviating hippocampal pathological injury， and upregulating the expression of PGC-1α/Nrf1/TFAM mRNA and Drp1/PINK1/Parkin signaling pathway-related proteins （P<0.05）. ConclusionJJXYS can significantly alleviate depressive-like behaviors and neurotransmitter imbalance in the rat model of PMD by regulating hippocampal MQC and upregulating the Drp1/PINK1/Parkin-related pathway. This study provides experimental evidence for the intervention of PMD with JJXYS.

ObjectiveTo analyze the incidence and spatiotemporal distribution of typhus fever in Baoshan City, Yunnan Province from 2005 to 2023, to identify high-risk populations and regions, so as to provide a scientific basis for optimizing the allocation of local prevention and control resources and developing targeted intervention measures. MethodsData of typhus fever cases in Baoshan City from 2005 to 2023 were obtained from the Infectious Disease Information Management System of the Chinese Center for Disease Control and Prevention. Descriptive epidemiological methods were used to analyze the temporal, spatial and demographic distribution of typhus fever cases. Spatial clustering was assessed using spatial dynamic window scan statistics (circular and elliptical windows), flexible spatial scan statistics, and local spatial autocorrelation methods (including local Moran’s I, local Geary’s C, and Getis-Ord G_i*). Retrospective spatiotemporal scan statistics were employed to detect spatiotemporal clusters. ResultsA total of 1 099 typhus fever cases were reported in Baoshan City from 2005 to 2023. The incidence rate peaked at 6.31/ 100 000 in 2007, followed by a decline until reaching its lowest level at 0.21/100 000 in 2015 , and subsequently rebounded during 2016‒2023. The highest proportion of cases was among children under 10 years of age (31.12%), and the top three occupations of cases were farmers, students, and children, accounting for 88.62% of all cases. Cases occurred predominantly between June and September each year. The incidence was relatively high in Jiucheng Town (62.58/100 000), Yaoguan Town (57.15/100 000), and Dianyang Town (46.81/100 000) of Shidian County. Spatial clustering analyses indicated that high-risk areas were mainly located in the southern part of Baoshan City, showing a south-to-north trend. Spatiotemporal scan analyses identified five clusters, with the most likely cluster centered around Yaoguan Town, covering ten towns (subdistricts) during the period 2007‒2010. ConclusionThe incidence of typhus fever in Baoshan City exhibits a clear seasonal and spatial clustering pattern, with peak incidence occurring in summer and autumn. Spatially, cases are primarily distributed in the southern part of Baoshan City, and high-risk clusters exhibit a south-to-north trend. Farmers, students, and children are the high-risk groups.

Objective To analyze the prevalence of hyperuricemia (HUA) among adults in Hebei Province and its influencing factors related to comorbidities with ^“three highs^”, and to provide a theoretical basis for the prevention and control of HUA and multi-disease co-management. Methods Data were derived from the 2018 China Chronic Disease and Risk Factors Surveillance program conducted in Hebei Province. A multi-stage stratified cluster random sampling method was used to select permanent residents aged ≥18 years. All statistical analyses were adjusted for complex weighting. Design-based logistic regression was employed to analyze factors influencing HUA prevalence, and ordinal logistic regression was used to analyze the influencing factors of HUA patients and their comorbidity with ^“three highs^”. Results The prevalence of HUA among adults in Hebei Province was 10.42%, with males showing higher rates than females (P<0.05). The highest prevalence of HUA was observed in the 18-39 age group, followed by a declining trend, and a resurgence in those aged ≥70 (P<0.05). Among HUA patients with comorbidities, isolated HUA, 1 comorbidity, 2 comorbidities, and 3 comorbidities accounted for 13.94%, 33.33%, 39.17%, and 13.56%, respectively. HUA combined with hypertension and dyslipidemia represented the highest proportion (31.07%). Analysis of the influencing factors of HUA revealed that higher education levels, obesity, central obesity, and dyslipidemia increased the risk of HUA (P<0.05). Ordinal logistic regression analysis of HUA combined with three highs showed that HUA patients aged ≥50 years, overweight individuals, and those with chronic kidney disease had a higher number of patients with three highs (P<0.05). Conclusion HUA exhibits insidious onset, and it is recommended to include uric acid testing in routine physical examinations. Targeted prevention measures, such as early uric acid testing and health education, should be implemented by Hebei authorities for populations with higher education levels, obesity, central obesity, and dyslipidemia to reduce HUA incidence. Additionally, health education and regular medical check-ups are recommended for overweight HUA patients and those with chronic kidney disease to prevent comorbidities and alleviate disease burden.

ObjectiveTo investigate the role of silent information regulatory protein （SIRT6）/hypoxia-inducible factor-1α （HIF-1α） pathway in regulating the reprogramming of glucose metabolism in ulcerative colitis （UC） and the mechanism of intervention of Shaoyaotang. MethodsForty-eight c57bL/6 mice were randomly divided into a blank group， a model group， a Mesalazine group （0.42 g·kg^-1）， a Shaoyaotang group （31.08 g·kg^-1）， an inhibitor group （OSS-128167， 50 mg·kg^-1）， and an inhibitor + Shaoyaotang group （50 mg·kg^-1 OSS-128167 + 31.08 g·kg^-1 Shaoyaotang）. A UC model was established by the administration of 2.5% dextran sulfate sodium （DSS） solution for mice in other groups for 7 d， except for the blank group. The mice in each group were treated with saline， Mesalazine， Shaoyaotang， inhibitor， and inhibitor + Shaoyaotang， respectively， for 7 d. The mice were necropsied 24 h after the last administration of the drug. The blood was collected from the orbital region， and colon tissue was taken. Hematoxylin-eosin （HE） staining was used to observe the pathological changes in colon tissue. Enzyme-linked immunosorbent assay （ELISA） was employed to detect serum interleukin （IL）-10， IL-17， and IL-6 levels. A biochemical method was used to detect glucose and lactate dehydrogenase A （LDHA） levels. Immunohistochemistry （IHC） was employed to detect IL-22 and transforming growth factor-β₁ （TGF-β₁） levels in colon tissue， and Western blot and real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） were used to detect relative protein and mRNA expressions of SIRT6， HIF-1α， and LDHA. ResultsCompared with those of the blank group， disease activity index （DAI） scores of mice in the model group and inhibitor group were significantly increased （P<0.01）. The length of colon tissue was significantly shortened， and colon tissue was congested and eroded. The pathohistological scores were significantly increased （P<0.01）. The levels of serum inflammatory factors IL-17 and IL-6 were significantly elevated， and the levels of IL-10 were significantly decreased （P<0.01）. The protein expressions of IL-22 and TGF-β₁ were significantly reduced in colon tissue （P<0.01）. The relative protein and mRNA expressions of SIRT6 were significantly decreased （P<0.01）， and the relative protein and mRNA expressions of HIF-1α and LDHA and the contents of glucose and lactate were significantly elevated （P<0.01）. The level of inflammation in the colon of the mice in the inhibitor group was more severe than that in the model group （P<0.01）. Compared with the model group， the Mesalazine group， the Shaoyaotang group， and the inhibitor + Shaoyaotang group showed reduced colonic injury， significant decrease in serum IL-17 and IL-6， significant increase in IL-10 （P<0.01）， significant increase in the protein expressions of IL-22 and TGF-β₁ in colon tissue （P<0.01）， significant increase in the protein expressions of SIRT6 and the relative mRNA expressions （P<0.01）， and significant reduction in the protein expressions of HIF-1α and LDHA， the relative mRNA expressions， and the contents of glucose and lactate （P<0.01）. Compared with those in the Shaoyaotang group， the serum IL-17 and IL-6 were significantly increased， and IL-10 was significantly decreased in the inhibitor + Shaoyaotang group （P<0.01）. The protein expressions of IL-22 and TGF-β₁ in colon tissue were significantly decreased （P<0.01）. The expressions of SIRT6 protein and the relative mRNA expressions were significantly decreased （P<0.01）. The protein expressions of HIF-1α and LDHA， the relative mRNA expressions， and the contents of glucose and lactate were significantly elevated （P<0.01）. However， the difference between the Shaoyaotang group and the Mesalazine group was not significant. ConclusionShaoyaotang can effectively treat DSS-induced mice with UC through the SIRT6/HIF-1α pathway， and its mechanism of action may be related to the regulation of the SIRT6/HIF-1α pathway and glucose metabolism reprogramming and the inhibition of glycolysis.

ObjectiveTo investigate the role of silent information regulatory protein （SIRT6）/hypoxia-inducible factor-1α （HIF-1α） pathway in regulating the reprogramming of glucose metabolism in ulcerative colitis （UC） and the mechanism of intervention of Shaoyaotang. MethodsForty-eight c57bL/6 mice were randomly divided into a blank group， a model group， a Mesalazine group （0.42 g·kg^-1）， a Shaoyaotang group （31.08 g·kg^-1）， an inhibitor group （OSS-128167， 50 mg·kg^-1）， and an inhibitor + Shaoyaotang group （50 mg·kg^-1 OSS-128167 + 31.08 g·kg^-1 Shaoyaotang）. A UC model was established by the administration of 2.5% dextran sulfate sodium （DSS） solution for mice in other groups for 7 d， except for the blank group. The mice in each group were treated with saline， Mesalazine， Shaoyaotang， inhibitor， and inhibitor + Shaoyaotang， respectively， for 7 d. The mice were necropsied 24 h after the last administration of the drug. The blood was collected from the orbital region， and colon tissue was taken. Hematoxylin-eosin （HE） staining was used to observe the pathological changes in colon tissue. Enzyme-linked immunosorbent assay （ELISA） was employed to detect serum interleukin （IL）-10， IL-17， and IL-6 levels. A biochemical method was used to detect glucose and lactate dehydrogenase A （LDHA） levels. Immunohistochemistry （IHC） was employed to detect IL-22 and transforming growth factor-β₁ （TGF-β₁） levels in colon tissue， and Western blot and real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） were used to detect relative protein and mRNA expressions of SIRT6， HIF-1α， and LDHA. ResultsCompared with those of the blank group， disease activity index （DAI） scores of mice in the model group and inhibitor group were significantly increased （P<0.01）. The length of colon tissue was significantly shortened， and colon tissue was congested and eroded. The pathohistological scores were significantly increased （P<0.01）. The levels of serum inflammatory factors IL-17 and IL-6 were significantly elevated， and the levels of IL-10 were significantly decreased （P<0.01）. The protein expressions of IL-22 and TGF-β₁ were significantly reduced in colon tissue （P<0.01）. The relative protein and mRNA expressions of SIRT6 were significantly decreased （P<0.01）， and the relative protein and mRNA expressions of HIF-1α and LDHA and the contents of glucose and lactate were significantly elevated （P<0.01）. The level of inflammation in the colon of the mice in the inhibitor group was more severe than that in the model group （P<0.01）. Compared with the model group， the Mesalazine group， the Shaoyaotang group， and the inhibitor + Shaoyaotang group showed reduced colonic injury， significant decrease in serum IL-17 and IL-6， significant increase in IL-10 （P<0.01）， significant increase in the protein expressions of IL-22 and TGF-β₁ in colon tissue （P<0.01）， significant increase in the protein expressions of SIRT6 and the relative mRNA expressions （P<0.01）， and significant reduction in the protein expressions of HIF-1α and LDHA， the relative mRNA expressions， and the contents of glucose and lactate （P<0.01）. Compared with those in the Shaoyaotang group， the serum IL-17 and IL-6 were significantly increased， and IL-10 was significantly decreased in the inhibitor + Shaoyaotang group （P<0.01）. The protein expressions of IL-22 and TGF-β₁ in colon tissue were significantly decreased （P<0.01）. The expressions of SIRT6 protein and the relative mRNA expressions were significantly decreased （P<0.01）. The protein expressions of HIF-1α and LDHA， the relative mRNA expressions， and the contents of glucose and lactate were significantly elevated （P<0.01）. However， the difference between the Shaoyaotang group and the Mesalazine group was not significant. ConclusionShaoyaotang can effectively treat DSS-induced mice with UC through the SIRT6/HIF-1α pathway， and its mechanism of action may be related to the regulation of the SIRT6/HIF-1α pathway and glucose metabolism reprogramming and the inhibition of glycolysis.

ObjectiveTo investigate the effect of Shaoyaotang on T helper cell 17/regulatory T lymphocyte（Th17/Treg） cell balance in ulcerative colitis and decipher the intervention mechanism based on glucose metabolism reprogramming. MethodsThe mouse model of ulcerative colitis was established by the dextran sulfate sodium （DSS） method. Forty-eight C57BL/6 mice were randomly allocated into normal， model， Western drug control （mesalazine， 0.39 g·kg^-1·d^-1）， Shaoyaotang （15.54 g·kg^-1·d^-1）， inhibitor （2-deoxy-D-glucose， 2-DG， 100 mg·kg^-1·d^-1）， and inhibitor （2-DG， 100 mg·kg^-1·d^-1） + Shaoyaotang （15.54 g·kg^-1·d^-1） groups. Mice were administrated with the corresponding drugs by gavage for 7 days. The general conditions and the colon injury degree were observed 24 h after the last administration. The expression of interleukin （IL）-10 and IL-17 in the colon tissue was detected by immunohistochemical staining. Western blot and Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） were performed to determine the protein and mRNA levels， respectively， of hypoxia-inducing factor-1α （HIF-1α）， lactate dehydrogenase （LDHA）， and hexokinase 2 （HK2） in the colon tissue. Th17/Treg cell differentiation was detected by flow cytometry. Enzyme-linked immunosorbent assay was employed to measure the levels of lactic acid and glucose in the colon tissue and IL-10， IL-17， and IL-6 in the serum. ResultsCompared with the normal group， the model group showed decreases in body weight and disease activity index （DAI） （P<0.05）， elevations in levels of HIF-1α， LDHA， HK2， IL-17， IL-6， Th17 cells， lactic acid， and glucose in the colon tissue （P<0.05）， and declines in the levels of of IL-10 and Treg cells （P<0.05）. Compared with the model group， the drug administration groups showed increases in body weight and DAI （P<0.05）， declines in levels of HIF-1α， LDHA， HK2， IL-17， IL-6， Th17 cells， lactic acid， and glucose in the colon tissue （P<0.05）， and rises in levels of IL-10 and Treg cells （P<0.05）. Shaoyaotang+2-DG group had the most obvious effect. ConclusionShaoyaotang can relieve diarrhea and bloody stool in mice with ulcerative colitis by restoring the Th17/Treg cell balance via regulation of glucose metabolism reprogramming， thus playing a role in the treatment of ulcerative colitis.

ObjectiveTo explore the regulation of Shaoyaotang on glucose metabolism reprogramming of macrophages and the mechanism of this decoction in inhibiting macrophage polarization toward the M1 phenotype. MethodsHuman monocytic leukemia-1 （THP-1） cells were treated with 100 ng·L^-1 phorbol myristate acetate for induction of macrophages as the normal control group. The cells treated with 100 ng·L^-1 lipopolysaccharide combined with 20 ng·L^-1 interferon （IFN）-γ for induction of M1-type macrophages were taken as the M1 model group. M1-type macrophages were treated with the blank serum， Shaoyaotang-containing serum， 0.5 mol·L^-1 2-deoxy-D-glucose （2-DG）， and Shaoyaotang-containing serum + 2-DG， respectively. After intervention， the expression of CD86 and CD206 was examined by flow cytometry. The levels of interleukin （IL）-6， tumor necrosis factor （TNF）-α， IL-10， and transforming growth factor （TGF）-β were assessed by ELISA. Real-time PCR and Western blot were employed to determine the mRNA and protein levels， respectively， of hypoxia-inducible factor-1 alpha （HIF-1α）， glucose transporter 1 （GLUT1）， hexokinase 2 （HK2）， glyceraldehyde-3-phosphate dehydrogenase （GAPDH）， and 6-phosphofructo-2-kinase/fructose-2，6-bisphosphatase 3 （PFKFB3）. ResultsCompared with that in the normal control group， the expression of CD86， the marker of M1-type macrophages， increased in the M1 model group and blank serum group （P<0.01）， which indicated that the M1 inflammatory model was established successfully. In addition， the M1 model group was observed with up-regulated mRNA and protein levels of proinflammatory cytokines IL-6 and TNF-α and glycolysis-related factors HIF-1α， GLUT1， HK2， GAPDH， and PFKFB3 （P<0.01）. Compared with the M1 model group， the Shaoyaotang-containing serum， 2-DG， and combined intervention groups showed decreased expression of CD86 （P<0.01）， down-regulated mRNA and protein levels of proinflammatory factors IL-6 and TNF-α and glycolysis-related factors HIF-1α， GLUT1， HK2， GAPDH， and PFKFB3 produced by M1-type macrophages （P<0.01）， increased expression of CD206 （marker of M2-type macrophages） （P<0.01）， and elevated levels of IL-10 and TGF-β produced by M2-type macrophages （P<0.01）. ConclusionShaoyaotang inhibits macrophage differentiation toward pro-inflammatory M1-type macrophages and promotes the differentiation toward anti-inflammatory M2-type macrophages by regulating glucose metabolism reprogramming. The evidence gives insights into new molecular mechanisms and targets for the treatment of ulcerative colitis with Shaoyaotang.

ObjectiveTo investigate the effect of Shaoyaotang on T helper cell 17/regulatory T lymphocyte（Th17/Treg） cell balance in ulcerative colitis and decipher the intervention mechanism based on glucose metabolism reprogramming. MethodsThe mouse model of ulcerative colitis was established by the dextran sulfate sodium （DSS） method. Forty-eight C57BL/6 mice were randomly allocated into normal， model， Western drug control （mesalazine， 0.39 g·kg^-1·d^-1）， Shaoyaotang （15.54 g·kg^-1·d^-1）， inhibitor （2-deoxy-D-glucose， 2-DG， 100 mg·kg^-1·d^-1）， and inhibitor （2-DG， 100 mg·kg^-1·d^-1） + Shaoyaotang （15.54 g·kg^-1·d^-1） groups. Mice were administrated with the corresponding drugs by gavage for 7 days. The general conditions and the colon injury degree were observed 24 h after the last administration. The expression of interleukin （IL）-10 and IL-17 in the colon tissue was detected by immunohistochemical staining. Western blot and Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） were performed to determine the protein and mRNA levels， respectively， of hypoxia-inducing factor-1α （HIF-1α）， lactate dehydrogenase （LDHA）， and hexokinase 2 （HK2） in the colon tissue. Th17/Treg cell differentiation was detected by flow cytometry. Enzyme-linked immunosorbent assay was employed to measure the levels of lactic acid and glucose in the colon tissue and IL-10， IL-17， and IL-6 in the serum. ResultsCompared with the normal group， the model group showed decreases in body weight and disease activity index （DAI） （P<0.05）， elevations in levels of HIF-1α， LDHA， HK2， IL-17， IL-6， Th17 cells， lactic acid， and glucose in the colon tissue （P<0.05）， and declines in the levels of of IL-10 and Treg cells （P<0.05）. Compared with the model group， the drug administration groups showed increases in body weight and DAI （P<0.05）， declines in levels of HIF-1α， LDHA， HK2， IL-17， IL-6， Th17 cells， lactic acid， and glucose in the colon tissue （P<0.05）， and rises in levels of IL-10 and Treg cells （P<0.05）. Shaoyaotang+2-DG group had the most obvious effect. ConclusionShaoyaotang can relieve diarrhea and bloody stool in mice with ulcerative colitis by restoring the Th17/Treg cell balance via regulation of glucose metabolism reprogramming， thus playing a role in the treatment of ulcerative colitis.

ObjectiveTo explore the regulation of Shaoyaotang on glucose metabolism reprogramming of macrophages and the mechanism of this decoction in inhibiting macrophage polarization toward the M1 phenotype. MethodsHuman monocytic leukemia-1 （THP-1） cells were treated with 100 ng·L^-1 phorbol myristate acetate for induction of macrophages as the normal control group. The cells treated with 100 ng·L^-1 lipopolysaccharide combined with 20 ng·L^-1 interferon （IFN）-γ for induction of M1-type macrophages were taken as the M1 model group. M1-type macrophages were treated with the blank serum， Shaoyaotang-containing serum， 0.5 mol·L^-1 2-deoxy-D-glucose （2-DG）， and Shaoyaotang-containing serum + 2-DG， respectively. After intervention， the expression of CD86 and CD206 was examined by flow cytometry. The levels of interleukin （IL）-6， tumor necrosis factor （TNF）-α， IL-10， and transforming growth factor （TGF）-β were assessed by ELISA. Real-time PCR and Western blot were employed to determine the mRNA and protein levels， respectively， of hypoxia-inducible factor-1 alpha （HIF-1α）， glucose transporter 1 （GLUT1）， hexokinase 2 （HK2）， glyceraldehyde-3-phosphate dehydrogenase （GAPDH）， and 6-phosphofructo-2-kinase/fructose-2，6-bisphosphatase 3 （PFKFB3）. ResultsCompared with that in the normal control group， the expression of CD86， the marker of M1-type macrophages， increased in the M1 model group and blank serum group （P<0.01）， which indicated that the M1 inflammatory model was established successfully. In addition， the M1 model group was observed with up-regulated mRNA and protein levels of proinflammatory cytokines IL-6 and TNF-α and glycolysis-related factors HIF-1α， GLUT1， HK2， GAPDH， and PFKFB3 （P<0.01）. Compared with the M1 model group， the Shaoyaotang-containing serum， 2-DG， and combined intervention groups showed decreased expression of CD86 （P<0.01）， down-regulated mRNA and protein levels of proinflammatory factors IL-6 and TNF-α and glycolysis-related factors HIF-1α， GLUT1， HK2， GAPDH， and PFKFB3 produced by M1-type macrophages （P<0.01）， increased expression of CD206 （marker of M2-type macrophages） （P<0.01）， and elevated levels of IL-10 and TGF-β produced by M2-type macrophages （P<0.01）. ConclusionShaoyaotang inhibits macrophage differentiation toward pro-inflammatory M1-type macrophages and promotes the differentiation toward anti-inflammatory M2-type macrophages by regulating glucose metabolism reprogramming. The evidence gives insights into new molecular mechanisms and targets for the treatment of ulcerative colitis with Shaoyaotang.