Role of kallistatin in protecting hepatic stellate cells against oxidation through inhibition of oxidative stress and activation of Akt-eNOS signaling
10.16438/j.0513-4870.2017-0199
- VernacularTitle:Kallistatin通过Akt-eNOS信号通路对肝星状细胞氧化损伤的保护作用
- Author:
Xiao-ping HUANG
1
;
Xiao WANG
2
;
Xiao-lan XIE
1
;
Wen-tao XU
1
;
Hui-yong YANG
2
;
Zhao-fa LI
2
;
Jun-sheng LIN
2
;
Yong DIAO
2
Author Information
1. College of Chemical Engineering and Materials Sciences, Quanzhou Normal University, Quanzhou 362000, China
2. Institute of Molecular Medicine, Huaqiao University, Quanzhou 362021, China
- Publication Type:ORIGINAL ARTICLES
- Keywords:
kallistatin;
hepatic stellate cell;
oxidation damage;
liver fibrosis
- From:
Acta Pharmaceutica Sinica
2017;52(9):1397-1403
- CountryChina
- Language:Chinese
-
Abstract:
The present study was aimed to investigate the role and mechanisms of kallistatin in protection against oxidative stress-induced hepatic stellate cell damage. The effects of kallistatin on the viability, the intracellular superoxide level and Akt, eNOS molecules were investigated in human hepatic stellate cell line LX-2 and the incompletely activated primary rat hepatic stellate cells. Two different oxidative-stress related models, the hydrogen peroxide model and the iron-overload model were used in the experiments. The results show that kallistatin protected the hepatic stellate cells from oxidative damage and repaired the cell damage by oxidative stress. The main mechanism is antioxidant activity of kallistatin, which can remove the oxidized substances inside the cells. On the other way, kallistatin activates Akt and eNOS molecules to generate the antioxidant effect. Our results help to explore new anti-fibrotic targets.
