Mechanisms of immunogenic cell death induced by octyl ester derivative of ginsenoside Rh2 in hepatocellular carcinoma cells based on endoplasmic reticulum stress
10.3969/j.issn.1000-484X.2024.04.016
- VernacularTitle:人参皂苷辛酸酯通过内质网应激诱导肝癌细胞免疫原性细胞死亡的机制研究
- Author:
Zhenzhen DAI
1
;
Qingxin HUANG
;
Qirui HU
;
Hancheng WU
;
Yao PAN
;
Zeyuan DENG
;
Fang CHEN
Author Information
1. 南昌大学公共卫生学院,南昌 330006
- Keywords:
Ginsenoside Rh2;
Octyl ester derivatives;
Hepatocellular carcinoma;
Immunogenic cell death;
Endoplasmic reticulum stress
- From:
Chinese Journal of Immunology
2024;40(4):767-771,779
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate whether octyl ester derivative of ginsenoside Rh2(Rh2-O)can induce immunogenic cell death of Huh-7 hepatocellular carcinoma cells and possible mechanism.Methods:Huh-7 cells were cultured in vitro,and divided into control group,Rh2-O group,positive control group(mitoxantrone treatment).Viability and apoptosis of cells were detected by CCK-8 and flow cytometry,respectively.Concentrations of high mobility family protein 1(HMGB1)and adenosine triphosphate(ATP)in supernatant were detected by ELISA and chemiluminescence assay,respectively.Membrane eversion of calreticulin(CRT)was detected by immunofluorescence assay.ROS level in cells was detected by fluorescence probe DCFH-DA,and expressions of proteins associated with endoplasmic reticulum stress signaling pathway were detected by Western blot.Results:Rh2-O treatment significantly reduced cell viability,promoted apoptosis,induced secretion of HMGB1,ATP,membrane eversion of CRT,increased accumulation of ROS in cells,and enhanced expressions of endoplasmic reticulum stress-related proteins PERK,eIF2α,p-eIF2α(all P<0.05).After addition of endoplasmic reticulum stress inhibitor 4-phenylbutyric acid(4-PBA),membrane eversion of CRT induced by Rh2-O was significantly inhibited(P<0.05).Conclusion:Rh2-O can induce immunogenic cell death in hepatocellular carcinoma cells,whose mechanism may be associated with activation of endoplasmic reticulum stress and promotion of CRT membrane eversion.
