CFTR suppressing hyperhomocysteinemia-induced hepatocyte damage in ApoE-/-mice
10.3969/j.issn.1006-5725.2016.10.007
- VernacularTitle:CFTR抑制ApoE－／－鼠高同型半胱氨酸血症诱导的肝损伤
- Author:
Yun JIAO
;
Anning YANG
;
Yue SUN
;
Fanqi KONG
;
Xiaoling YANG
;
Minghao ZHANG
;
Shaoju JING
;
Yideng JIANG
- Publication Type:Journal Article
- Keywords:
Hyperhomocysteinemia;
Cystic fibrosis transmembrane conductance regulator;
Hepatocel-lular injury;
ApoE-/-mice
- From:
The Journal of Practical Medicine
2016;32(10):1574-1577
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the function of CFTR in ApoE-/- mice with HHcy-induced hepato-cellular injury. Methods Thirty six 5-week old ApoE-/- mice were divided into three groups , including the ApoE-/- group, the HHcy group and the intervention group, (n = 12). Twelve normal C57BL/6J mice were fed with regular mouse diet as the normal control (SPF grade). HL-7702 human liver cells were intervened by Hcy (100 μmol/L) and 100 μmol/L Hcy + folic acid (100 μmol/L Hcy + F). The changes of Hcy, ALT and AST in the serum and the expression of CFTR mRNA and protein in liver and liver cells were detected. The concen-trations of ALT and AST in the liver cell intervened by VX-770 agonist and CFTR(inh)-172 inhibitor were mea-sured by ELISA. Results Compared with the control group , the levels of Hcy , ALT and AST were higher and the levels of CFTR mRNA and protein were lower in the Meth group (P < 0. 05 ) , while the reverse result in the Meth + F group (P < 0.05). Compared with the control group, the levels of CFTR mRNA and protein were de-creased and the levels of ALT and AST were increased in the 100 μmol/L Hcy group (P < 0.05). Compared with the 100 μmol/L Hcy group , the levels of CFTR mRNA and protein were increased and the levels of ALT and AST were decreased in the 100 μmol/L Hcy + F group (P < 0.05). Stimulated with VX-770 can reduce the concentrations of ALT and AST and the vice versa in the CFTR (inh)-17 group the concentration was increased in liver cells. Conclusion CFTR plays an important role in the regulation of hepatocellular injury by HHcy.
