Effect of sodium glycosaminodeoxycholate on apoptosis of hepatic stem cells in cholestatic microenvironment
10.16098/j.issn.0529-1356.2019.06.008
- Author:
Zhi-Peng LI
1
Author Information
1. Department of Hepatology, Children's Hospital of Chongqing Medical University
- Publication Type:Journal Article
- Keywords:
Cholestatic cirrhosis;
Liver stem cell;
Mouse;
Sodium glycosaminodeoxycholate;
Western blotting
- From:
Acta Anatomica Sinica
2019;50(6):747-753
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effects of hepatic stem cells survival in the pathological microenvironment of cholestatic cirrhosis, and the effects of sodium glycosaminodeoxycholate (GCDC) on apoptosis of hepatic stem cells in vitro. Methods: Balb/c mice were subjected to bile duct ligation (BDL) to simulate the pathological environment of cholestatic cirrhosis; Liver stem cells HP 14-19 were transplanted back into liver by the splenic vein and survival of cell colonization was detected; Effects of sodium glycosaminodeoxycholate on the viability of HP 14-19 cells at different concentrations by cell counting kit-8(CCK-8) and crystal violet staining, flow cytometry was used to detect the apoptosis of HP14-19 cells treated with 600 μmol/L GCDC 24 hours later, and the expression of Bax, Bcl-2, Capase-3, phosphorylated adenosine 5′-monophosphate-activated protein kinase α (p-AMPKα) and adenosine 5′-monophosphate-activated protein kinase α (AMPKα) were detected by Western blotting. Results: The results of CCK-8 and crystal violet staining showed that the proliferation of HP 14-19 cells was inhibited with the increase of the concentration of sodium glycosaminodeoxycholate. Flow cytometry showed that the apoptosis rate of GCDC treated group was higher than that of control group. Compared with the control group, the expression of Bax, Capase-3 was up-regulated and the expression of Bcl-2 protein was down-regulated in the experimental group. The results showed that GCDC could induce apoptosis of HP14-19 (P<0.05) AMPK was activated. Conclusion: Microenvironment of cholestatic cirrhosis induced apoptosis of liver stem cells.
