Objective:To investigate the protective effect of Akebia saponin D(ASD)on non-alcoholic fatty liver disease(NAFLD)in rats by regulating IL-6/STAT3 axis.Methods:Fifty SD rats were separated into control group,model group,low dose ASD group(ASD 20 mg/kg),high dose ASD group(ASD 40 mg/kg)and inhibitor group(ASD 40 mg/kg+IL-6/STAT3 signal pathway inhibitor LMT-28 3 mg/kg),with 10 rats in each group.Rats in control group were fed with standard diet,while the other four groups were fed with high fat and high sugar diet.All rats were fed for 6 consecutive weeks,and the corresponding dose of drugs was injected intraperitoneally from the 7th week,which were given drugs for 8 consecutive weeks.All rats were weighed to calculate liver index;levels of serum total cholesterol(TC),alanine aminotransferase(ALT),aspartate aminotransferase(AST)and triglyceride(TG)were mea-sured by automatic biochemical analyzer;HE staining was used to observe pathological changes of rats liver;oil red staining was used to observe lipid accumulation in rats liver;expressions of IL-6,JAK1,STAT3 in rats liver were detected by qRT-PCR;Western blot was used to detect expressions of IL-6,JAK1,p-JAK1,STAT3 and p-STAT3 proteins.Results:Compared with control group,hepatocytes in liver tissue of model group were swollen,accompanied by many ballooning changes,severe cytoplasmic vacuolization,the structure of hepatic lobule was unclear,and accompanied by inflammatory cell infiltration,and obvious red granular lipid droplets occupied most of the cytoplasm,body mass,liver index,levels of serum TC,ALT,AST,TG,expressions of IL-6,JAK1,STAT3 mRNAs,and IL-6,p-JAK1/JAK1,p-STAT3/STAT3 proteins in liver tissue of rats were obviously increased(P<0.05);compared with model group,damage of hepatic lobule structure in low and high doses ASD groups were reduced,swelling and vacuolization of liver cells were reduced,and accumulation of lipid droplets in liver tissue was obviously reduced.Body mass,liver index,levels of serum TC,ALT,AST and TG in rats were obviously decreased(P<0.05),while expressions of IL-6,JAK1,STAT3 mRNAs and IL-6,p-JAK1/JAK1,p-STAT3/STAT3 proteins in liver tissue were further increased(P<0.05);LMT-28,an inhibitor of IL-6/STAT3 signaling pathway,attenuated the liver protective effect of ASD on NAFLD rats.Conclusion:ASD can protect liver of NAFLD rats by activating IL-6/STAT3 signaling pathway.

Objective:To investigate the protective effect of Akebia saponin D(ASD)on non-alcoholic fatty liver disease(NAFLD)in rats by regulating IL-6/STAT3 axis.Methods:Fifty SD rats were separated into control group,model group,low dose ASD group(ASD 20 mg/kg),high dose ASD group(ASD 40 mg/kg)and inhibitor group(ASD 40 mg/kg+IL-6/STAT3 signal pathway inhibitor LMT-28 3 mg/kg),with 10 rats in each group.Rats in control group were fed with standard diet,while the other four groups were fed with high fat and high sugar diet.All rats were fed for 6 consecutive weeks,and the corresponding dose of drugs was injected intraperitoneally from the 7th week,which were given drugs for 8 consecutive weeks.All rats were weighed to calculate liver index;levels of serum total cholesterol(TC),alanine aminotransferase(ALT),aspartate aminotransferase(AST)and triglyceride(TG)were mea-sured by automatic biochemical analyzer;HE staining was used to observe pathological changes of rats liver;oil red staining was used to observe lipid accumulation in rats liver;expressions of IL-6,JAK1,STAT3 in rats liver were detected by qRT-PCR;Western blot was used to detect expressions of IL-6,JAK1,p-JAK1,STAT3 and p-STAT3 proteins.Results:Compared with control group,hepatocytes in liver tissue of model group were swollen,accompanied by many ballooning changes,severe cytoplasmic vacuolization,the structure of hepatic lobule was unclear,and accompanied by inflammatory cell infiltration,and obvious red granular lipid droplets occupied most of the cytoplasm,body mass,liver index,levels of serum TC,ALT,AST,TG,expressions of IL-6,JAK1,STAT3 mRNAs,and IL-6,p-JAK1/JAK1,p-STAT3/STAT3 proteins in liver tissue of rats were obviously increased(P<0.05);compared with model group,damage of hepatic lobule structure in low and high doses ASD groups were reduced,swelling and vacuolization of liver cells were reduced,and accumulation of lipid droplets in liver tissue was obviously reduced.Body mass,liver index,levels of serum TC,ALT,AST and TG in rats were obviously decreased(P<0.05),while expressions of IL-6,JAK1,STAT3 mRNAs and IL-6,p-JAK1/JAK1,p-STAT3/STAT3 proteins in liver tissue were further increased(P<0.05);LMT-28,an inhibitor of IL-6/STAT3 signaling pathway,attenuated the liver protective effect of ASD on NAFLD rats.Conclusion:ASD can protect liver of NAFLD rats by activating IL-6/STAT3 signaling pathway.

Objective:Rapid assessment of the outcome after percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS) is an important clinical issue. In this study, an electrocardiogram (ECG) analysis method based on dynamic learning was proposed.Methods:A total of 203 patients with ACS after successful PCI were enrolled for prospective analysis at the Emergency Department of Qilu Hospital of Shandong University from April 2019 to December 2020. All patients were divided into group without ≥70% postoperative stenosis ( n=72) and group with ≥ 70% postoperative stenosis ( n=131) according to the presence of 70% or more stenosis after PCI. The clinical data of ACS patients were collected and analyzed by χ2 test, t-test, or Mann-Whitney test. ECGs were recorded before and 2 h after PCI, and were dynamically analyzed to generate cardiodynamicsgram (CDG) using dynamic learning. In the group without ≥ 70% postoperative stenosis, the model and CDG index for evaluating myocardial ischemia were obtained by training support vector machine (SVM) using 10 times 10-fold cross-validation. Results:There was no significant difference in clinical data between the two groups. The prediction accuracy and sensitivity of the support vector machine model for myocardial ischemia in group without≥70% postoperative stenosis were 73.61%, and 84.72% respectively. CDG transformed from disorderly to regular after PCI, and CDG index decreased significantly ( P<0.001): 90.28% (65) patients in group without≥70% postoperative stenosis, and 79.39% (104) patients in group with≥70% postoperative stenosis had lower CDG indexes than before PCI. Conclusions:In this study, CDG obtained by dynamic learning can intuitively and effectively evaluate the changes of myocardial ischemia before and after PCI, which is helpful to assist clinicians to formulate the next treatment plan.

Objective To investigate the tumor-inhibitory effect of cytokine-induced killer cells(CIK)co-cul-tured with dendritic cells (DC)pulsed by breast cancer stem cell antigen on the same tumor-bearing mice. Methods Breast cancer stem cells were isolated from the cell line of MCF-7/ADR and extract lyses antigen of the stem cell was saved. DC and CIK derived from peripheral blood mononuclear cells of healthy individuals were co-cultured and pulsed or un-pulsed by the above antigen lyses. This DC+CIK were injected to breast tumorbearing mice (BCSC-AP-DC+CIK group), and were used to compared with the common breast cancer cell antigen (rather than breast cancer stem cell antigen) pulsed DC+CIK group(AP-DC+CIK group), DC+CIK group, CIK CIK group and normal saline group(NS group). The tumor-inhibitory effect were evaluated and compared among all 5 groups through the tumor size, TdT-mediated dUTP nick end labeling test (TUNEL), examining expression level of bcl-2 and bax by immunohistochemistry. Results The tumor size in each group before and after therapy and the tumor size after therapy between each group was of significant difference(P＜0.05). The maximum size is NS group(3.625±0.093)cm3 and BCSC-AP-DC+CIK group is minimum,which is (1.234±0.131)cm3. BC-SC-AP-DC+CIK group is of highest expression of bax and apoptotic index value, lowest bcl-2 expression in all 5 groups. Conclusion The CIK co-cultured with DC pulsed breast cancer stem cell antigen was more effective to induce apoptosis of breast cancer cells than those of CIK cells co-cultured with DC pulsed breast cancer cell antigen,CIK cells co-cultured with DC and CIK cells.