1.Advances in the effect of adenosine A2 receptor activation in the prevention and treatment of ischemic diseases
Yahan SUN ; Mali HE ; Jingman XU
Clinical Medicine of China 2018;34(2):173-176
Adenosine,also known as adenine nucleoside,is an important bioactive substances. A large number of studies found that adenosine is involved in the prevention and treatment of many diseases by activating adenosine receptors. Up to now,Adenosine receptors have cloned four subtypes,such as A1,A2a,A2b and A3 and they can be combined with AD and start the downstream signal transduction mechanism,then have different effects on the body. This article will summarize the distribution and activation of adenosine A2 receptor and its role and mechanism in the prevention and treatment of disease.
2.Role of mitochondrial permeability transition pore in mediating the inhibitory effect of gastrodin on oxidative stress in cardiac myocytes .
Xuechao HAN ; Jingman XU ; Sen XU ; Yahan SUN ; Mali HE ; Xiaodong LI ; Xinyu LI ; Jiayi PI ; Rui YU ; Wei TIAN
Journal of Southern Medical University 2018;38(11):1306-1311
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.
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
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Myocytes, Cardiac
;
drug effects
;
metabolism
;
Oxidative Stress
;
Reactive Oxygen Species
;
analysis