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作 者:靳趁心[1] 刘冰[1] 乔治向 陈东来[1] 王永兰[1]
机构地区:[1]天津医科大学口腔医院牙周科,天津300070 [2]合肥市口腔医院,安徽合肥230601
出 处:《牙体牙髓牙周病学杂志》2013年第11期677-680,共4页Chinese Journal of Conservative Dentistry
基 金:天津医科大学科学基金(2011KY31)
摘 要:目的:研究β-防御素3(HBD3)调节人牙龈成纤维细胞(HGFs)分泌MMP-1和PGE2的信号通路。方法:取P5代HGFs接种于96孔板,并随机分为1个对照组(HBD3)和7个实验组(HBD3+antiTLR2、HBD3+anti-TLR4、HBD3+SB203580、HBD3+PD98059、HBD3+SP600125、HBD3+LY294002、HBD3+SC3060)。各实验组分别以相应的信号通路抑制剂anti-TLR2、anti-TLR4预处理30 min,SB203580、PD98059、SP600125、LY294002、SC3060预处理60min,然后各组再加入100μL浓度为1μg/mL的HBD3进行培养,12h后收集各组培养上清液,ELISA法检测MMP-1及PGE2浓度。结果:信号通路抑制剂SB203580、PD98059、SC3060、anti-TLR2各组MMP-1的浓度(ng/mL)分别为3.660±0.286、3.410±0.554、4.435±0.235、3.995±0.612,低于对照组(5.128±0.256)ng/mL(P<0.05);信号通路抑制剂SP600125、SC3060两组PGE2浓度(pg/mL)分别为146.518±15.800和180.349±5.490,低于对照组(209.213±7.284)pg/mL(P<0.05)。结论:HBD3调节HGFs分泌MMP-1涉及TLR2、P38、ERK、NF-κB信号途径;调节PGE2分泌涉及JNK和NF-κB信号途径。AIM: To investigate the signaling pathways in human beta-defensins 3 (HBD3) -induced prostaglandin E2 ( PGE2 ) and matrix metalloproteinase- 1 ( MMP- 1 ) production in human gingival fibroblasts ( HG- Fs). METHODS: HGFs of passage 5 were cultured in 96-well culture plates. After reached to sub-confluence, the cells were pretreated with signaling pathway inhibitors including anti - TLR2, anti - TLR4, SB203580, PD98059, SP600125, LY294002 and SC3060 respectively. Cells without inhibitor treatment served as the controls. The ceils were further incubated with 1 μg/mL HBD3 for 12 h and the MMP-1 and PGE2 concentrations in the supernatant were meas- ured by ELISA . RESULTS : In the group of SB203580, PD98059, SC3060, anti - TLR2 and control MMP - 1 con- centratrion (ng/mL) was 3. 660 ± 0. 286, 3. 410 ±0. 554, 4. 435 ± 0. 235, 3. 995 ± 0.612 and 5. 128 ± 0.256 respec- tively( each experimental group vs control, P 〈 0.05 ). In the group of SP600125, SC3060 and control PGE2 concentra- tion (pg/mL) was 146. 518 ± 15. 800, 180. 349 ± 5. 490 and 209. 213 ± 7. 284 respectively ( vs control, P 〈 0.05 ). CONCLUSION: ERK, p38, NF-κB, and TLR2 signaling pathways are involved in HBD3-regulated MMP-1 production, while JNK and NF-κB signaling pathways are involved in HBD3-regulated PGE2 production in HGFs.
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