AIM:To investigate the potential of atractylenolide Ⅲ(AⅢ)in mitigating dextran sulfate sodium(DSS)-induced injury in a mouse model of chronic inflammatory bowel disease(IBD),and to explore the mechanisms in-volved,particularly the modulation of signal transducer and activator of transcription 3(STAT3)signaling,which plays a crucial role in the homeostasis of T helper 17(Th17)and regulatory T(Treg)cells.METHODS:A mouse model of DSS-induced chronic IBD was established,and the mice were divided into 4 groups:control,model(DSS),high-dose(50 mg/kg)AⅢ,and low-dose(30 mg/kg)AⅢ.The disease activity index(DAI)was utilized to assess disease severity.Histo-pathological damage in the colons of IBD mice was evaluated by hematoxylin-eosin(HE)staining.The protein levels of phosphorylated STAT3,occludin and zonula occludens-1(ZO-1)were analyzed using immunohistochemical staining and Western blot.Flow cytometry was employed to examine the differentiation of splenic lymphocytes into Th17/Treg cells.RESULTS:Both DAI assessments and HE staining indicated that AⅢ significantly alleviated inflammatory injury in mice with DSS-induced chronic IBD.Immunohistochemical analysis demonstrated that AⅢ enhanced the expression of ZO-1 and occludin in colonic tissues.Flow cytometry results revealed that AⅢ helped maintain the balance between splenic Th17 and Treg cells.Furthermore,immunohistochemical staining and Western blot showed that AⅢ inhibited the phos-phorylation of STAT3.CONCLUSION:Treatment with AⅢ effectively reduced inflammatory injury in a mouse model of chronic IBD by preserving Th17/Treg homeostasis through the inhibition of STAT3 phosphorylation.As a natural com-pound,AⅢ exhibits significant therapeutic potential for the treatment of chronic IBD.

AIM:To investigate the potential of atractylenolide Ⅲ(AⅢ)in mitigating dextran sulfate sodium(DSS)-induced injury in a mouse model of chronic inflammatory bowel disease(IBD),and to explore the mechanisms in-volved,particularly the modulation of signal transducer and activator of transcription 3(STAT3)signaling,which plays a crucial role in the homeostasis of T helper 17(Th17)and regulatory T(Treg)cells.METHODS:A mouse model of DSS-induced chronic IBD was established,and the mice were divided into 4 groups:control,model(DSS),high-dose(50 mg/kg)AⅢ,and low-dose(30 mg/kg)AⅢ.The disease activity index(DAI)was utilized to assess disease severity.Histo-pathological damage in the colons of IBD mice was evaluated by hematoxylin-eosin(HE)staining.The protein levels of phosphorylated STAT3,occludin and zonula occludens-1(ZO-1)were analyzed using immunohistochemical staining and Western blot.Flow cytometry was employed to examine the differentiation of splenic lymphocytes into Th17/Treg cells.RESULTS:Both DAI assessments and HE staining indicated that AⅢ significantly alleviated inflammatory injury in mice with DSS-induced chronic IBD.Immunohistochemical analysis demonstrated that AⅢ enhanced the expression of ZO-1 and occludin in colonic tissues.Flow cytometry results revealed that AⅢ helped maintain the balance between splenic Th17 and Treg cells.Furthermore,immunohistochemical staining and Western blot showed that AⅢ inhibited the phos-phorylation of STAT3.CONCLUSION:Treatment with AⅢ effectively reduced inflammatory injury in a mouse model of chronic IBD by preserving Th17/Treg homeostasis through the inhibition of STAT3 phosphorylation.As a natural com-pound,AⅢ exhibits significant therapeutic potential for the treatment of chronic IBD.

Teicoplanin is a glycopeptide antibiotic for treatment of gram-positive bacterial infections in children, especially for methicillin-resistant staphylococcus aureus infection.The body clearance of teicoplanin differs between child and adult.This article explores the suitable testing indicators based on the clinical medication guide and the latest research progress , as well as the pharmacokinetic and pharmacodynamics of teicoplanin , to provide information for individualized dosage regime of teicoplanin in children.

Objective The population -based study was conducted in Hebei Renqiu 60 -70 years old resi-dents to evaluate cardiovascular disease morbidity risk in next 10 years,to analyze the related risk factors and provide an objective basis for the prevention and control of cardiovascular diseases in the local areas.Methods Cluster sam-pling method was used to select elderly residents (aged from 60 to 70 years)in Renqiu city as the research subjects. A total of 5 010 cases,2 163 males,2 847 females were included in this study.Investigation contents included health questionnaire,anthropometric and laboratory detection.According to the Framingham Risk Score (FRS),10 -year risk probability of cardiovascular disease was calculated.Research subjects were divided into low risk group (<10%),medium risk group (≥10% and <20%),high -risk group (≥20%),and logistic regression was used to analyze the risk degree of the related risk factors.Results The 10 -year cardiovascular risk median value of 60 -70 years elderly residents was 8.0 (4.0 -16.0),among them male was 16.0 (12.0 -20.0),female was 4.0 (2.0 -6.0).Low risk group had 2 784 cases,accounted for 55.7%;medium risk group had 1 452 cases,accounted for 29.0%,high-risk group had 774 cases,accounted for 15.3%.The most important risk factors were smoking and cholesterol increasing,who contributes elderly residents aged 60 to 70 years in Renqiu cardiovascular 10 -year risk.The history of stroke,excessive drinking,waist circumference,diastolic blood pressure,elevated uric acid level and HOMA -IR were the independent risk factors in moderately high risk 10 -year probability of cardiovascular.Conclusion The elderly residents aged 60 to 70 years in Renqiu has higher cardiovascular risk of 10 years.Quitting smoking,limitting alcohol,controlling of blood pressure,blood lipids,uric acid,waist circumference and HOMA -IR are important to improve cardiovascular 10 -year risk.Among them,quit smoking and alcohol limit are the most effective measures.

Objective To investigate the expression of the hypoxia-inducible factor (HIF)-1α in rat brain neurons and the intervention of β-sodium aescinate after restoration of spontaneous circulation (ROSC).Methods Sixty SD adult rats were randomly (random number) divided into 3 groups (n =20),namely experiment group,control group and sham operation group.(1) The rats of experiment group were injected intraperitoneally with β-sodium aescinate (5 mg/kg) immediately after ROSC.(2) The rats of control group received normal saline injected intraperitoneally instead of β-sodium aescinate solution.(3)The rats of sham operation group did not have cardiac arrest and β-sodium aescinate intervention.Cardiac arrest rat model was established by using asphyxiation and intra-venous potassium chloride solution.Blood samples were taken 1 h,6 h,12 h and 24 h after ROSC,and subsequently rats were sacrificed and their brain tissues were harvested.The expressions of HIF-1 α mRNA,vascular endothelial growth factor (VEGF)mRNA and erythropoitin (EPO) mRNA and their protein levels in rat brain neurons were detected by using RT-PCR and immunohistochemistry,and the levels of serum neuron-specific enolase (NSE) and S100β proteins were determined by using enzyme-linked immunosorbent assay.The t test or one-way ANOVA was used to assess overall differences among groups for each of the variables,followed by Bonferroni test for multiple comparisons.Pearson method was used for correlation analysis.Results Compared with the sham operation group at intervals of 1 h,6 h,12 h and 24 h after ROSC,levels of serum S100β and NSE proteins were significantly increased in rats of the control group (P ＜ 0.05).Meanwhile,the expressions of HIF-1 α mRNA,VEGF mRNA and EPO mRNA and their protein levels in rat brain neurons were significantly increased in the control rats (P ＜0.05).Compared with the control group at intervals of 1 h,6 h,12 h and 24 h after ROSC,levels of serum NSE and S100β proteins were significantly decreased in rats of the experiment group (P ＜ 0.05).Whereas,the expressions of HIF-1 α mRNA,VEGF mRNA and EPO mRNA and their protein levels in rat brain neurons were significantly increased in rats of the experiment group (P ＜0.05).HIF-1 α mRNA was positively correlated with EPO mRNA and VEGF mRNAs (r =O.866,P ＜0.05 ; r =0.952,P ＜ O.01).Conclusions The expression of hypoxia-inducible factor-1 α is increased in rat brain cells after ROSC,and β-sodium aescinate up-regulates the expression of hypoxia-inducible factor1 α mRNA and protein levels.The up-regulated expression of hypoxia-inducible factor-1α improves the resistance of brain cells to ischemia and hypoxia contributing neuronal protection,which might be due to upregulated EPO and VEGF expressions induced by hypoxia-inducible factor-1α.

Objective To investigate the neutrophil elastase (NE) in patients with acute lung injury (ALI)/acute respiratory distress syndrome (ARDS).Methods Thirty-six patients of ALI/ARDS and 16 healthy volunteers(control group)were involved in the study.The patients of ALI/ARDS were divided into three groups:group A (the oxygenation index was 201-300 mm Hg,1 mm Hg=0.133 kPa),group B (150-200 mm Hg),and group C (<150 mm Hg).The NE in serum and bronchoalveolar Lavage fluid (BALF) were measured.Results The NE in the serum and BALF in group A [(1.76±0.63)nmol/L and (1.67±0.59)nmol/L],group B [(3.26±0.51)nmol/L and (3.64±0.56)nmol/L] and group C [(4.56 ±0.68)nmol/L and (4.62±0.39)nmol/L] were much higher than that in control group [(0.67±0.54)nmol/L and (0.62±0.48)nmol/L].The NE in the serum and BALF of dead patients were higher than that in patients who were alive.Moreover,the NE in the patients of ALI/ARDS was inversely related to the oxygenation index (r=-0.901,P＜0.01). Conclusion The NE in patients of ALI/ARDS is higher than that in healthy people,and it is significantly related to the severity and the prognosis of ALI/ARDS.