Study on the protective effect and mechanism of astragaloside Ⅳ on radiation-induced esophageal epithelial cell injury
ZHANG Jianhua
LI Xiaofei
LI Guijun
LI Mingli
YUAN Lei
Abstract：Objective To investigate the protective effect of astragaloside IV on radiation-induced esophageal epithelial cell(Het-1A)injury and explore its underlying mechanism.Methods A radiation-induced esophagitis model was established by irradiating Het-1A cells with 6MV-X-rays(2,4,6 Gy).The model cells were treated with different concentrations of astragaloside IV(0,5,10,20,40,80,160 μmol/L).Cell proliferation was assessed using the CCK-8 method to determine the optimal intervention concentration.Het-1A cells were divided into the following groups:normal control group,radiation injury model group,astragaloside IV(40 μmol/L)group,phosphatidylinositol 3-kinase(PI3K)inhibitor LY294002(10 μmol/L)group,and astragaloside IV(40 μmol/L)+LY294002(10 μmol/L)group.The levels of tumour necrosis factor-α(TNF-α)and interleukin-6(IL-6)were measured by ELISA.The cell proliferation was evaluated using the EdU method.The apoptosis was detected by flow cytometry,phosphorylated PI3K(p-PI3K)protein expression was assessed by immunofluorescence,and the expression of caspase-3,Bcl-2,Bax,PI3K,protein kinase B(AKT),mammalian target of rapamycin(mTOR),and their cleaved or phosphorylated proteins were determined by Western blotting.Results A radiation-induced Het-1A injury cell model was constructed using a 4 Gy radiation dose.Compared with the 0 μmol/L astragaloside IV group,the viability of radiation-injured Het-1A cells treated with 10,20,40,and 80 μmol/L astragaloside IV was significantly increased(P<0.05).Compared with the normal control group,the radiation injury model group exhibited elevated levels of TNF-α,IL-6,apoptosis rate,cleaved caspase-3/caspase-3,and Bax protein,as well as reduced cell proliferation rate,Bcl-2,p-PI3K/PI3K,p-AKT/AKT,and p-mTOR/mTOR protein levels(P<0.05).Compared with the radiation injury model group,the astragaloside IV group showed significantly reduced levels of the aforementioned inflammatory factors,apoptosis rate,and related pro-apoptotic protein expression,while the proliferation ability and the phosphorylation levels of proteins related to the PI3K/AKT/mTOR pathway were increased(P<0.05).Compared with astragaloside IV group,astragaloside IV+LY294002 group showed significantly increased inflammatory response,apoptosis level,and pro-apoptotic protein expression,while the proliferation ability and activation level of the PI3K/AKT/mTOR pathway were decreased(P<0.05),suggesting that LY294002 could inhibit the protective effect of astragaloside IV on radiation-injured Het-1A cells.Conclusion Astragaloside IV can alleviate 6MV-X-ray-induced Het-1A cell injury,promote cell proliferation,and suppress inflammatory responses and apoptosis.Its mechanism may be related to the activation of the PI3K/AKT/mTOR pathway.
Keywords：astragaloside Ⅳradiation-induced esophagitisproliferationapoptosisPI3K/AKT/mTOR pathway
Publication Date：2025-11-28
Online Publishing Date：2026-01-05(First online date of this platform, not the publication date of the document)
Pages：6( 1074-1079 )