Effects of Cu/Zn SOD mediated by cell penetrating peptide 4 on hypoxia/reoxygenation injury in myocardial cells
10.3969/j.issn.1671-8348.2017.21.001
- VernacularTitle:细胞穿透肽4介导的Cu/Zn SOD对缺氧复氧损伤心肌细胞的影响
- Author:
Yu WANG
;
Qing LI
;
Wenjing ZENG
;
Jingyi CHEN
;
Juying LIU
- Keywords:
superoxide dismutase;
cell penetrating peptide;
anoxia;
injuries;
myocardium
- From:
Chongqing Medicine
2017;46(21):2881-2883,2888
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effect of cell-penetrating peptide (protein transduction domain 4,PTD4) mediated copper-zinc superoxide dismutase (Cu/Zn SOD) on hypoxia/reoxygenation injury (HRI) in rat myocardial cells.Methods Rat myocardial cell H9C2 HRI model was prepared by using the anaerobic incubator (85% N2,10% H2,5% CO2).The HRI group (without adding any treating factor in HRI cell culture fluid),HRI+Cu/Zn SOD group (adding 10 μmol/L Cu/Zn SOD) and HRI+PTD4-Cu/Zn SOD group (10 μmol/L PTD4-Cu/Zn SOD) were set up.In addition,normally cultured myocardial cells served as the normal control group.After incubating for 30 min,the ultra microstructure of mitochondria was observed under transmission electron microscope.The mitochondrial membrane potential was detected by JC-1 kit.The myocardial cell apoptosis was detected by TdT mediated dUTP nick end labeling TUNEL technique.Results The mitochondria injury degree after 30 min incubation in the PTD4-Cu/Zn SOD group was significantly improved compared with the HRI group.Compared with the normal control group,the mitochondrial membrane potential in the HRI group was significantly decreased,while the mitochondrial membrane potential in the PTD4-Cu/Zn SOD group was lower than that in the normal control group,but compared with the HRI group,which was obviously recovered.The cardiomyocyte apoptosis in the HRI+PTD4-Cu/Zn SOD group was (10.20±2.77)%,which was significantly decreased compared with (28.40±2.41)% in the HRI group,the difference was statistically significant (P<0.05).Conclusion PTD4 mediated Cu/Zn SOD can attenuate HRI in rat myocardial cells.
