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XCT-790 对沉默DKK1、Sost 腺病毒载体转染MG63 细 胞中OPG、CTGF、FGF2、TNFα 的影响研究.
- Source :
-
Chinese Journal of Osteoporosis . Jul2017, Vol. 23 Issue 7, p841-845. 5p. - Publication Year :
- 2017
-
Abstract
- Objective To investigate the effect of ERRα inhibitor ( XCT-790 ) on silencing Dickkopf1 ( DKK1 ) ,sclerostin ( Sost) reconmbinant adenovirus vector,and the related proteins OPG,CTGF,FGF2,and TNFα in the transfection MG63 cells. Methods MG63 cells were divided into control group,silence DKK1 group,silence Sost group,silence ( DKK1 + Sost) group, XCT-790 dispose no-load adenovirus group,XCT-790 dispose silence DKK1 group,XCT-790 dispose silence Sost group,and XCT-790 dispose silence ( DKK1 + Sost) group. The silencing DKK1 or Sost reconmbinant adenovirus vector was transfected to MG63 cells,respectively. The expression levels of related proteins OPG,CTGF,FGF2,and TNFα were detected with Western blotting in MG63 cells. Results ( 1) Compared with control group,the expression levels of OPG,CTGF,FGF2 increased in silence DKK1,Sost,and DKK1 + Sost group ( P < 0. 05 ) ,while the expression level of TNFα decreased ( P < 0. 05 ) . The expression levels of OPG,CTGF,and FGF2 decreased ( P < 0. 05) ,while TNFα increased ( P < 0. 05) ,when XCT-790 intervened MG63 cells. ( 2) Compared with silence DKK1,Sost,and DKK1 + Sost group,the increased expression levels of OPG,CTGF, FGF2 were impaired ( P < 0. 05) and the decreased expression level of TNFα increased ( P < 0. 05) in XCT-790 dispose silence DKK1,Sost,and DKK1 + Sost groups. Conclusion XCT-790 decreases the expression levels of OPG,CTGF,and FGF2, increases the expression level of TNFα. It also regulates the changed expression levels of OPG,CTGF,FGF2,and TNFα in silencing DKK1,Sost,and DKK1 + Sost MG63 cells. [ABSTRACT FROM AUTHOR]
Details
- Language :
- Chinese
- ISSN :
- 10067108
- Volume :
- 23
- Issue :
- 7
- Database :
- Academic Search Index
- Journal :
- Chinese Journal of Osteoporosis
- Publication Type :
- Academic Journal
- Accession number :
- 124714445
- Full Text :
- https://doi.org/10.3969/j.issn.1006-7108.2017.07.001