Objective To investigate the effect of β-catenin on the osteogenic differentiation of human periodontal ligament stem cells (PDLSCs) under mechanical tension.Methods PDLSCs were seperately cultured in vitro from the periodontium attached at freshly extracted teeth.β-catenin-targeting agonist or inhibitor was applied to the PDLSCs to upregulate or downregulate the expression of activity of β-catenin protein.The expression of β-catenin protein and the osteogenetic related markers(ALP,BMP2,Runx 2) under the mechanical tension with different period(0,6,12,24 h) were assessed with Western blot in the PDLSCs irritated with agonist or inhibitor.Results Compared with the PDLSCs without mechanical tension,the expression of osteogenesis related marker proteins,ALP and Runx 2,in PDLSCs were enhanced under the circular mechanial tensile stress (P ＜ 0.05).In the PDLSCs irritated with WAY-262611,the β-catenin-targeting agonist,the expression of osteogenetic related markers ALP in the PDLSCs was improved during the first 12 h period of mechnical tensile load,which was significantly higher than that in the DMSO group.Conclusion Wnt/β-catenin signaling pathway plays an important role in the early osteogenesis differentiation of PDLSCs under cyclic tension.The β-catenin promotes osteogenic differentiation of PDLSCs under mechanical tension.

AIM To explore the effects of glycyrrhetinic acid on the gastric ulcer rats infected by Helicobacter pylori (Hp) and its action mechanism.METHODS Gastric ulcer rat models were induced by acetic acid stress and then followed by Hp infection.After treatment with low and high doses of glycyrrhetinic acid,the ulcer index,gastric acid and proteinase activities in gastric ulcer rats were analyzed.The effects of glycyrrhetinic acid on the expressions of BCL2 and Caspase-3,the GSK3β activity in gastric mucosa and gastric epithelial cells,and the cell apoptosis level were then detected.RESULTS Glycyrrhetinic acid reduced the ulcer index,gastric acid and proteinase activities in rats.Besides,the expression of BCL2 was significantly up-regulated by glycyrrhetinic acid in gastric mucosa and gastric epithelial cells,whereas the expression of Caspase-3,level of cell apoptosis,and GSK3β activity were significantly reduced.After the treatment with GSK3 β activator LY294002,the level of BCL2 was down-regulated,Caspase-3 expression was increased,and the level of cell apoptosis was enhanced.CONCLUSION Glycyrrhetinic acid promotes the healing of gastric ulcer infected by Hp via regulating GSK3β activity and inhibiting apoptosis of gastric epithelial cells.

Objective To investigate infection status and antimicrobial resistance mechanism of methicillin-resistant Staphylococcusaureus(MRSA),and provide reference for the rational antimicrobial use in clinic. Methods Staphylococcusaureus (SA)isolated from various specimens in Xuzhou area in 2012-2015 were collected,MR-SA strains were preliminarily screened by cefoxitin disk diffusion method,and confirmed by amplification of mecA gene,antimicrobial resistance of MRSA was determined by Kirby-Bauer method,minimal inhibitory concentration (MIC)was measured by E-test method,genotypes of staphylococcal chromosomal cassette mec(SCCmec)were de-termined by multiplex PCR. Results A total of 116 strains of MRSA were identified among 210 SA strains in 2012-2015,114 of which were positive for mecA gene,the total detection rate of MRSA was 55.24% . Susceptibility rates of MRSA to vancomycin,quinupristin/dalfopristin,and linezolid were all 100% ,resistance rates of MRSA to chloramphenicol and furantoin were both low,which were 15.52% and 1.72% respectively,resistance rates of MR-SA to 10 kinds of antimicrobial agents were all>80% ;resistance rates of MRSA to penicillins,aminoglycosides, macrolides,quinolones,sulfanilamide,rifampicin,tetracycline,and clindamycin were all higher than methicillin-sensitive Staphylococcusaureus(MSSA). MICs of vancomycin to MRSA in 2012-2015 were all 1.0μg/mL,MIC90 were all 1.5μg/mL,one MRSA isolate was with a vancomycin MIC of 2.0μg/mL in 2015. MRSA typing results of 116 MRSA isolates showed that SCCmec II,SCCmec III,and SCCmec IV accounted for 9.48% (n= 11),73.28% (n= 85),and 1.72% (Iva,n= 2;IVb,n= 2)respectively,13.79% (n= 16)of MRSA isolates were nontypeable, SCCmec I and SCCmec V type strains were not found. Conclusion MRSA is seriously multidrug-resistant,the drift has not been discovered in MIC value of vancomycin against MRSA,the major SCCmec genotype of MRSA is SCCmec III,infection control measures should be taken to control MRSA infection.

[ ABSTRACT] AIM:To investigate the effect of artemisinin on lipopolysaccharide ( LPS)-induced intestinal epi-thelial barrier damage in IEC-6 cells and its molecular mechanism.METHODS:Cultured IEC-6 cells were divided to 5 groups:control group, LPS (100 mg/L) group and LPS +Artemisinin (30, 50 and 100μmol/L) groups.The cytotoxici-ty was detected by MTT assay.The releases of TNF-α, IL-1βand IL-6 in the IEC-6 cells were measured by ELISA.The transepithelial electrical resistance ( TER) was detected by electrical resistance tester, and the horseradish peroxidase (HRP) flux permeability were analyzed by a microplate reader.The expression of tight junction proteins, ZO-1, claudin-1 and occludin, and the expression of TLR4/MyD88/NF-κB at mRNA and protein levels were determined by RT-qPCR and Western blot.RESULTS:Artemisinin alone (up to 100 μmol/L) or in combination with LPS (100 mg/L) was not toxic to IEC-6 cells.Compared with control group, the releases of TNF-α, IL-1βand IL-6 in the culture supernatant of IEC-6 cells significantly increased after treatment with LPS.The expression of TLR4/MyD88/NF-κB was activated by LPS.LPS down-regulated the protein expression of ZO-1, claudin-1 and occludin.However, artemisinin treatment decreased the re-leases of TNF-α, IL-1βand IL-6 in the culture supernatant of IEC-6 cells.The expression of TLR4/MyD88/NF-κB at mR-NA and protein levels was gradually reduced after treatment with artemisinin.In addition, artemisinin upregulated the pro-tein expression of ZO-1, claudin-1 and occludin significantly (P<0.01) in a dose-dependent manner.CONCLUSION:Artemisinin attenuates LPS-induced intestinal epithelial barrier damage by inhibiting TLR4/MyD88/NF-κB activation in the IEC-6 cells.