Relationship of PI3K/Akt signaling pathway and the activation of hepatic stellate cells and its role in radiation-induced hepatic fibrosis
10.3760/cma.j.issn.0254-5098.2015.09.003
- VernacularTitle:PI3K/Akt信号通路与肝星状细胞活化的关系及其在放射性肝纤维化中的作用
- Author:
Xiaoxu LUO
;
Lei XIAO
;
Ge WU
;
Yunlian WANG
;
Hua ZHANG
;
Yongxing BAO
- Publication Type:Journal Article
- Keywords:
X-rays;
Hepatic stellate cells;
Radiation-induced hepatic fibrosis;
PI3K/Akt signaling pathway
- From:
Chinese Journal of Radiological Medicine and Protection
2015;35(9):652-656
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the relationship of PI3K/Akt signaling pathway with the activation of hepatic stellate cells (HSC) and its role in radiation-induced hepatic fibrosis.Methods HSC was treated with 6 MV X-ray irradiation (IR) together with the inhibitor of PI3K/Akt signaling pathway.The cells were divided into inhibitor group,10 Gy IR group,10 Gy + inhibitor group,20 Gy IR group,an 20 Gy + inhibitor group and blank control group.Then cell apoptosis rate was detected,the expression of transforming growth factor β1 (TGF-β1) in cell supernatant and the mRNA expressions of α-smooth muscle actin (α-SMA) and phosphorylation protein kinase B (p-Akt) were measured.Results Compared with the control group,the apoptosis rate of 10 and 20 Gy IR group increased with irradiation dose (t =8.43,11.63,P ＜0.05) but they were reduced by the inhibitor of PI3K/Akt (t =8.09,4.88,P ＜0.05).The expressions of TGF-β1,α-SMA,and p-Akt also increased with irradiation dose (t =6.91,7.80,9.28,P＜0.05) but they were declined by this inhibitor for both 10 Gy IR (t =6.17,15.11,10.34,P＜0.05) and 20 Gy IR (t =10.04,6.85,23.84,P＜0.05).Conclusions X-ray irradiation could activate HSC through PI3K/Akt signaling pathway,which may further result in hepatic fibrosis.
