Role of mitochondrial permeability transition pore in mediating the inhibitory effect of gastrodin on oxidative stress in cardiac myocytes .
10.12122/j.issn.1673-4254.2018.11.05
- Author:
Xuechao HAN
1
;
Jingman XU
1
;
Sen XU
1
;
Yahan SUN
1
;
Mali HE
1
;
Xiaodong LI
1
;
Xinyu LI
1
;
Jiayi PI
1
;
Rui YU
1
;
Wei TIAN
1
Author Information
1. Medical Research Center (International Scientific and Technological Cooperation Base of Geriatrics Medicine), North China University of Science and Technology, Tangshan 063000, China.
- Publication Type:Journal Article
- Keywords:
cyclosporin;
gastrodin;
mitochondrial permeability transition pore;
oxidative stress injury
- MeSH:
Adenosine Triphosphate;
analysis;
Apoptosis;
drug effects;
Benzyl Alcohols;
antagonists & inhibitors;
pharmacology;
Caspase 3;
analysis;
Cell Line;
Cell Survival;
drug effects;
Cyclosporine;
pharmacology;
Cytochromes c;
analysis;
Glucosides;
antagonists & inhibitors;
pharmacology;
Humans;
Hydrogen Peroxide;
antagonists & inhibitors;
pharmacology;
Membrane Potential, Mitochondrial;
drug effects;
Mitochondrial Membrane Transport Proteins;
physiology;
Myocytes, Cardiac;
drug effects;
metabolism;
Oxidative Stress;
Reactive Oxygen Species;
analysis
- From:
Journal of Southern Medical University
2018;38(11):1306-1311
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To explore the role of mitochondrial permeability transition pore (mPTP) in mediating the protective effect of gastrodin against oxidative stress damage in H9c2 cardiac myocytes.
METHODS:H9c2 cardiac myocytes were treated with HO, gastrodin, gastrodin+HO, cyclosporin A (CsA), or CsA+gas+HO group. MTT assay was used to detect the survival ratio of H9c2 cells, and flow cytometry with Annexin V-FITC/PI double staining was used to analyze the early apoptosis rate after the treatments. The concentration of ATP and level of reactive oxygen species (ROS) in the cells were detected using commercial kits. The mitochondrial membrane potential of the cells was detected with laser confocal microscopy. The expression of cytochrome C was detected with Western blotting, and the activity of caspase-3 was also assessed in the cells.
RESULTS:Gastrodin pretreatment could prevent oxidative stress-induced reduction of mitochondrial membrane potential, and this effect was inhibited by the application of CsA. Gastrodin significantly lowered the levels of ROS and apoptosis-related factors in HO-exposed cells, and such effects were reversed by CsA. CsA significantly antagonized the protective effect of gastrodin against apoptosis in HO-exposed cells.
CONCLUSIONS:Gastrodin prevents oxidative stress-induced injury in H9c2 cells by inhibiting mPTP opening to reduce the cell apoptosis.
