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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.

Authors :
李钊政
万雷
乔荣勤
彭鹏豪
肖本浩
刘少津
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