YANG Yang, LIU Ting, WANG Wen-hua, et al. Protective Effect of Shenxiong Glucose Injection on HO-induced Oxidative Damage of H9c2 Cells[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(8): 153-158.
YANG Yang, LIU Ting, WANG Wen-hua, et al. Protective Effect of Shenxiong Glucose Injection on HO-induced Oxidative Damage of H9c2 Cells[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(8): 153-158. DOI: 10.13422/j.cnki.syfjx.2016080153.
Objective: To investigate the protective effect of Shenxiong Glucose Injection (SGI) on H2O2-induced oxidative damage of H9c2 cells. Method: The in vitro oxidative stress damage model was established by treating H9c2 cells with H2O2(300 μmol·mL-1) for 0.5 h. SGI-pretreated group:pretreated H9c2 cells with SGI (100
200
400 μmol·mL-1) for 6 h. Blank group and model group were treated additionally with H2O2 for 0.5 h. The intracellular reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were detected by flow cytometry. The cell viability was detected by MTS assay;ELISA methods was used to determine LDH release
MDA content
SOD
CAT
GSH-PX activity. The expression of apoptosis-related genes Caspase-3
Bax and Bcl-2 was detected by western blotting technology. Result: After H9C2 cells was treated with H2O2(300 μmol·mL-1) for 0.5 h
the survival rate of the cells decreased to about 50%. The experimental results were so appropriate and repeatable that the subsequent oxidative damage model was established under the conditions. Compared with the control group
the cells survival was significantly increased (P<0.05
P<0.01) by pretreating with SGI for 6 h. SGI not only decreased the release of LDH (P<0.05
P<0.01)
MDA (P<0.05
P<0.01)
but also increased the activity of SOD
GSH-PX
CAT (P<0.01). In addition
the content of ROS significantly decreased (P<0.01)
and MMP was increased (P<0.01). Western blot showed SGI can significantly enhance the expression of Bcl-2 and weaken the expression of Caspase-3(P<0.05
P<0.01). Conclusion: SGI shows the protective effect on H2O2-induced oxidative damage of H9c2 cells. Its mechanism may be correlated with increase in ROS removal ability and inhibition of apoptosis.