To explore the effects of exercise and Danzhi Jiangtang Capsule (DJC), a compound traditional herbal medicine, on the JNK signaling pathway in pancreatic tissues of diabetic rats and to investigate the possible mechanisms of exercise and DJC in treating diabetes.

Aim To study the characteristics of the binding reaction of Troxetutin with bovine serum albumin (BSA) by fluorescence and ultra violet-visible absorption spectra.Methods The quenching mechanism of the fluorescence of BSA by troxerutin was studied with fluorescence.To determine the dynamic quenching constants and static binding constants,the Stern-Volmer equation and the double reciprocal Lineweaver-Burk equation were applied. The number of binding site was calculated with double logarithmic equation and the main binding force was discussed by thermodynamic equations. The binding distance and energy transfer efficiency between donor (BSA) and acceptor (troxerutin) were obtained effectively quenched fluorescence of BSA via static quenching processes. The binding constant Ka was calculated to be in the order of 106,indicating a strong interaction between Troxerutin and BSA. The number of binding site was approximately equal to 1,the binding distance was 1.97 nm,the energy transfer efficiency was 0.529,and the binding force was mainly hydrophobic force.Conclusion Troxerutin effectively quenchs the intrinsic fluorescence of BSA via static quenching mechanism,and the binding is mainly driven by the hydrophobic interaction.

OBJECTIVETo establish a RP-HPLC method for simultaneous determination of phenylethanoid glycosides plantainoside D and verbascoside in Chirita longgangensis var. hongyao.

METHODThe analysis was performed on a Agilent C18 column (4.6 mm x 250 mm, 5 microm) with CH3CN-1% HAc (16:84)as mobile phase at a flow rate of 1.0 mL x min(-1), and at a column temperature of 30 degrees C. The detection wave length was 332 nm.

RESULTThe linear ranges of calibration of plantainoside D and verbascoside were 3.125-100.00 mg x L(-1) (r = 0.9998) and 25.00-500.0 mg x L(-1) (r = 0.9998). The average recoveries were 101.3% and 100.8% with RSD of 2.6% and 2.2% (n=9), respectively.

CONCLUSIONThe method is simple, accurate, reliable and can be used for the quality evaluation of C. longgangensis var. hongyao and its preparation.

Chromatography, High Pressure Liquid ; methods ; Chromatography, Reverse-Phase ; methods ; Coumaric Acids ; analysis ; Disaccharides ; analysis ; Glucosides ; analysis ; Magnoliopsida ; chemistry ; Phenols ; analysis ; Plant Extracts ; analysis ; Plant Stems ; chemistry

OBJECTIVE:To investigate the condition and characteristics of drug-induced liver injury (DILI) of anti-infective agents and provide reference for the prevention and treatment of anti-infective agents related DILI. METHODS:Based on retrospective analysis,a total of 572 DILI reports of anti-infective agents were collected from PLA ADR monitoring center during 2009 to 2013, and then analyzed statistically in terms of patient’s age and gender,main diagonosis,categories of DILI-inducing drugs,type,route of administration,occurrence time,lab indicator,DILI types and clinical manifestations,the application of liver protective drugs,out-comes,etc. RESULTS:Among 572 DILI cases,there were 412 cases(72.03%)of male patients and 160 cases(27.97%)of female patients,and average age of the patients was(44.54±23.75)years old. ADRs were related to 57 kinds of anti-infective agents in 6 cat-egories. Rifampin was the most frequent in suspected drugs,followed by isoniazid,moxifloxacin,fluconazole,azithromycin,cefurox-ime, cefoperazone/sulbactam, levofloxacin, cefoxitin and voriconazole. Intravenous infusion was the main administration route (74.48%). The occurrence time of ADRs was mainly within two weeks (86.19%). Hepatocellular damage (93.33%) was the main type in 360 cases of ADR for evaluation of liver injury types. The majority of cases(82.17%)were cured or improved after drug with-drawal and symptomatic treatment. CONCLUSIONS:Cephalosporin,fluoroquinolones,antituberculosis and antifungal drugs might be the common agents which caused liver injury. Hepatocellular damage is the most frequent type. Most of patients have a favourable prognosis. Clinical medical staffs should strengthen the awareness of DILI caused by anti-infective agents and ehance the prevetion of it.

Objective To investigate the mechanism mediating the regulatory effect of lncRNA MAGI2-AS3 on cisplatin(DDP)resistance in non-small cell lung cancer(NSCLC).Methods MAGI2-AS3 and miR-1269a expression levels were detected by qRT-PCR in DDP-sensitive lung cancer cell lines(A549 and H1299)and their resistant counterparts(A549/DDP and H1299/DDP).In A549 and H1299 cells with MAGI2-AS3 silencing and A549/DDP and H1299/DDP cells overexpressing MAGI2-AS3,the effects of 20 μmol/L DDP on cell viability and apoptosis were examined with CCK-8 assay,colony formation assay,flow cytometry and Western blotting,and the changes in epithelial-mesenchymal transition(EMT)were assessed with wound healing and Transwell assays.The interaction between MAGI2-AS3,miR-1269a and PTEN was predicted using GEPIA,StarBase and miRDB and verified with luciferase reporter gene assay and radioimmunoprecipitation(RIP)assay.A miR-1269a mimic and pcDNA3.1-PTEN plasmid were used to perform the rescue assay.Results MAGI2-AS3 expression was significantly downregulated in lung cancer tissues(P<0.05)in association with a poor prognosis(P<0.05).In the two DDP-resistant lung cancer cell lines,MAGI2-AS3 expression was significantly lowered as compared with the sensitive cells.Silencing MAGI2-AS3 significantly enhanced cell viability and promoted EMT of A549 and H1299 cells irrespective of DDP treatment,and also decreased DDP-induced apoptosis of the cells.In A549/DDP and H1299/DDP cells,MAGI2-AS3 overexpression strongly repressed cell viability and EMT irrespective of DDP treatment and promoted DDP-induced cell apoptosis.Luciferase reporter gene and RIP assays confirmed the binding of MAGI2-AS3 with miR-1269a and the binding of miR-1269a with 3'-UTR domain of PTEN.The rescue assay demonstrated that MAGI2-AS3 acted as a sponge for miR-1269a to promote PTEN expression and downregulate AKT phosphorylation,thus inhibiting EMT and promoting DDP-induced apoptosis of A549/DDP cells.Conclusion MAGI2-AS3 enhances DDP sensitivity of NSCLC by targeted regulation of the miR-1269a/PTEN/AKT signaling axis.

Objective To investigate the mechanism mediating the regulatory effect of lncRNA MAGI2-AS3 on cisplatin(DDP)resistance in non-small cell lung cancer(NSCLC).Methods MAGI2-AS3 and miR-1269a expression levels were detected by qRT-PCR in DDP-sensitive lung cancer cell lines(A549 and H1299)and their resistant counterparts(A549/DDP and H1299/DDP).In A549 and H1299 cells with MAGI2-AS3 silencing and A549/DDP and H1299/DDP cells overexpressing MAGI2-AS3,the effects of 20 μmol/L DDP on cell viability and apoptosis were examined with CCK-8 assay,colony formation assay,flow cytometry and Western blotting,and the changes in epithelial-mesenchymal transition(EMT)were assessed with wound healing and Transwell assays.The interaction between MAGI2-AS3,miR-1269a and PTEN was predicted using GEPIA,StarBase and miRDB and verified with luciferase reporter gene assay and radioimmunoprecipitation(RIP)assay.A miR-1269a mimic and pcDNA3.1-PTEN plasmid were used to perform the rescue assay.Results MAGI2-AS3 expression was significantly downregulated in lung cancer tissues(P<0.05)in association with a poor prognosis(P<0.05).In the two DDP-resistant lung cancer cell lines,MAGI2-AS3 expression was significantly lowered as compared with the sensitive cells.Silencing MAGI2-AS3 significantly enhanced cell viability and promoted EMT of A549 and H1299 cells irrespective of DDP treatment,and also decreased DDP-induced apoptosis of the cells.In A549/DDP and H1299/DDP cells,MAGI2-AS3 overexpression strongly repressed cell viability and EMT irrespective of DDP treatment and promoted DDP-induced cell apoptosis.Luciferase reporter gene and RIP assays confirmed the binding of MAGI2-AS3 with miR-1269a and the binding of miR-1269a with 3'-UTR domain of PTEN.The rescue assay demonstrated that MAGI2-AS3 acted as a sponge for miR-1269a to promote PTEN expression and downregulate AKT phosphorylation,thus inhibiting EMT and promoting DDP-induced apoptosis of A549/DDP cells.Conclusion MAGI2-AS3 enhances DDP sensitivity of NSCLC by targeted regulation of the miR-1269a/PTEN/AKT signaling axis.

Objective To explore the effect of mixed antibiotics on the intestinal flora of mice to affect the immune regulation of the body,explore the role of intestinal flora in the development of obesity,and provide new ideas and ways for the prevention and treatment of obesity.Methods Seventy-two 10-week-old male C57BL/6 mice were randomly divided into blank control(Ctrl)group,high-fat diet(HF)group,antibiotic(ABX)group,and combined(COMB)group(n=18).At the first 2 weeks(lavage intervention weeks),Ctrl and HF group were given normal saline gavage;ABX and COMB group were given mixed antibiotics gavage,and the gavage volume was 0.2 mL/animal/day.For the following 8 weeks(feeding weeks),Ctrl and ABX group were fed with ordinary diet,HF and COMB group were fed with high-fat diet.Body weight was measured weekly,and fasting blood glucose was measured before and after gavage,and at the 4th and 8th week of feeding.Oral glucose tolerance test was performed at the end of the experiment.The organ coefficient was measured and the cell morphology of white and brown adipose tissue was observed.Serum was collected for the determination of free fatty acid,high-density lipoprotein,low-density lipoprotein,triglyceride,and total cholesterol.Serum TNF-α,IL-10,IL-4,IL-13,IL-33 and MCP-1 was detected by ELISA.The stool of mice was collected for second generation sequencing.Results High-fat diet increased body weight,serum total cholesterol,low-density lipoprotein,IL-13,IL-33,TNF-α,MCP-1 content,and decreased glucose tolerance and organ coefficient in mice(P＜0.05).From the first feeding week to the end of the experiment,body weight in COMB group was significantly lower than that in HF group(P＜0.05).The level of glucose tolerance,serum total cholesterol,low density lipoprotein,IL-13,IL-33,TNF-α and MCP-1 in COMB group was lower than those in HF group(P＜0.05).The α diversity of intestinal flora in ABX group was lower than that in Ctrl group(P＜0.05).Congestion and bleeding in WAT were obvious in HF group,but not in COMB group.The microbial community composition of ABX and HF group was similar to that of Ctrl and COMB group,respectively.Conclusion High-fat diet induces obesity,disorder of glucose and lipid metabolism and inflammation in mice.Short-term mixed antibiotic use can regulate the intestinal flora of mice,mediate increased expression of related anti-inflammatory factors,up-regulate host immunity,and improve glucose and lipid metabolism in mice.

Objective:To examine the heritability of body mass index (BMI) and coronary heart disease (CHD), and to explore whether genetic factors can explain their correlation.Methods:Participants were from 11 provinces/municipalities reqistered in the Chinese National Twin Registry (CNTR) from 2010 to 2018. Participants data were collected from face-to-face questionnaire survey. Bivariate structure equation model was used to estimate the heritability and the genetic correlation of BMI and CHD.Results:A total of 20 340 pairs of same-sex twins aged ≥25 years were included in this study. After adjusting for age and gender, the heritability of BMI and CHD was 0.52 (95% CI: 0.49-0.55) and 0.76 (95% CI: 0.69-0.81), respectively. Further, a genetic correlation was identified between BMI and CHD ( rA=0.10, 95% CI:0.02-0.17). Conclusion:In Chinese adult twin population, BMI and CHD are affected by genetic factors, and their correlation can be attributed to the common genetic basis.

Objective:To examine the heritability of body mass index (BMI) and coronary heart disease (CHD), and to explore whether genetic factors can explain their correlation.Methods:Participants were from 11 provinces/municipalities reqistered in the Chinese National Twin Registry (CNTR) from 2010 to 2018. Participants data were collected from face-to-face questionnaire survey. Bivariate structure equation model was used to estimate the heritability and the genetic correlation of BMI and CHD.Results:A total of 20 340 pairs of same-sex twins aged ≥25 years were included in this study. After adjusting for age and gender, the heritability of BMI and CHD was 0.52 (95% CI: 0.49-0.55) and 0.76 (95% CI: 0.69-0.81), respectively. Further, a genetic correlation was identified between BMI and CHD ( rA=0.10, 95% CI:0.02-0.17). Conclusion:In Chinese adult twin population, BMI and CHD are affected by genetic factors, and their correlation can be attributed to the common genetic basis.

Objective To study the effects of antibiotics and high-fat diet on energy metabolism and the browning of white adipose tissue (WAT) and brown adipose tissue (BAT) in mice, so as to provide new ideas for the possible mechanism of adipose tissue in the prevention and treatment of obesity. Methods A total of 80 10-week-old C57BL/6 male mice were fed with normal diet in the early stage, and the antibiotic gavage group (AG) and antibiotic high-fat group (AFG) were given mixed antibiotics by gavage. The blank group (BG) and the high-fat diet group (FG) were given normal saline intragastric solution for 2 weeks, and after the gavage operation, the FG group and the AFG group were given high-fat diet for obesity modeling, and the BG group and AG group continued to be fed with normal diet for 8 weeks (N=20). After the experiment, each group was injected with β3-adrenergic receptor agonists for 5 days, and the high-fat/ordinary diet remained unchanged. At the end of the experiment, basal metabolic rate (BMR), fasting blood glucose (FBG) and rectal temperature were measured, and feces, blood, subcutaneous white fat, epididymis and brown adipose tissue in the scapular area of mice were collected. The automatic biochemical analyzer was used to determine the blood biochemical indexes; reverse transcription polymerase chain reaction (RT-qPCR) was used to measure the expression of genes related to browning of WAT and BAT adipose tissue, respectively. Real-time quantitative polymerase chain reaction (qPCR) was used to determine the expression of WAT mitochondrial DNA (mt DNA). Results From the 4th week to the end of the experiment, the weight of the AFG group was significantly higher than that of the AG group and significantly lower than that of the FG group (P<0.05). The body weight, organ coefficient, serum TC level, rectal temperature and WAT cell diameter in the AFG group were significantly higher than those in the AG group. The serum levels of FBG, TC and LDL in the AFG group were significantly lower than those in the FG group (P<0.05). The overall BMR(mlO2/h) FG group was significantly higher than that of BG group, and the AFG group was significantly higher than that of AG. BMR per unit body weight (mlO2/h/g) AFG was significantly higher than that of FG group (P<0.05). The expressions of RIP140, PPAR-γ and UCP-1 in BAT in the AFG group were significantly higher than those in the FG group, and the mt DNA copy number of WAT in the AFG group was significantly higher than that in the FG group (P<0.05). Conclusion Antibiotic intervention can up-regulate the expression of brown fat-related genes in high-fat diet mice, increase brown fat activity, increase the relative mitochondrial number of white fat, increase the level of browning of white fat, promote thermogenesis, increase the BMR per unit body weight of adult obese mice, and then improve the overall energy metabolism of the body, and slow down the weight gain induced by high-fat diet to a certain extent.