Ophiopogonin D protects cardiomyocytes against ophiopogonin D'-induced injury through suppressing endoplasmic reticulum stress.
10.19540/j.cnki.cjcmm.20190102.003
- Author:
Jia WANG
1
;
Ning-Ning WANG
2
;
Yun-Xuan GE
2
;
Hong-Ling TAN
2
;
Zeng-Chun MA
2
;
Yu-Guang WANG
2
;
Yue GAO
1
Author Information
1. Guangdong Pharmaceutical University Guangzhou 510006,China Institute of Radiation Medicine,Academy of Military Medical Sciences Beijing 100850,China.
2. Institute of Radiation Medicine,Academy of Military Medical Sciences Beijing 100850,China.
- Publication Type:Journal Article
- Keywords:
CYP2J3;
apoptosis;
endoplasmic reticulum stress;
ophiopogonin D;
ophiopogonin D'
- MeSH:
Apoptosis;
Cardiotonic Agents;
pharmacology;
Cells, Cultured;
Endoplasmic Reticulum Stress;
drug effects;
Humans;
Myocytes, Cardiac;
drug effects;
Saponins;
pharmacology;
Spirostans;
pharmacology
- From:
China Journal of Chinese Materia Medica
2019;44(9):1876-1881
- CountryChina
- Language:Chinese
-
Abstract:
This study is aimed to investigate the intervention effect and possible mechanism of ophiopogonin D( OPD) in protecting cardiomyocytes against ophiopogonin D'( OPD')-induced injury,and provide reference for further research on toxicity difference of saponins from ophiopogonins. CCK-8 assay was used to evaluate the effect of OPD and OPD' on cell viability. The effect of OPD on OPD'-induced cell apoptosis was measured by flow cytometry. Morphologies of endoplasmic reticulum were observed by endoplasmic reticulum fluorescent probe. PERK,ATF-4,Bip and CHOP mRNA levels were detected by Real-time quantitative polymerase chain reaction( PCR) analysis. ATF-4,phosphorylated PERK and e IF2α protein levels were detected by Western blot assay. RESULTS:: showed that treatment with OPD'( 6 μmol·L-1) significantly increased the rate of apoptosis; expressions of endoplasmic reticulum stress related genes were increased. The morphology of the endoplasmic reticulum was changed. In addition,different concentrations of OPD could partially reverse the myocardial cell injury caused by OPD'. The experimental results showed that OPD'-induced myocardial toxicity may be associated with the endoplasmic reticulum stress,and OPD may modulate the expression of CYP2 J3 to relieve the endoplasmic reticulum stress caused by OPD'.
