| Objectives:To study the mechanism of Chinese medicine monomer Danshentong IIA protection on myocardial ischemic/reperfusion injury, specifically to investigate the role of Notch pathway modulation in I/R induced oxidative stress and apoptosis.Methods:Culture the primary neonatal rat myocardiocytes, and establish a model of ischemic/reperfusion injury according to previous reports. Four groups were settled, including control group, SI/R group, DAPT+SI/R group and DanshentongⅡA+SI/R group. Myocardiocytes of SI/R group were incubated in DMEM medium for1h, then simulate ischemia for2hours, after that DMEM medium were utilized for reperfusion for4hours. DAPT+SI/R group was incubated with DMEM within DAPT for an hour, then treated with the ischemic/reperfusion injury procedure. Cells in Danshentong ⅡA+SI/R group were pretreated in DMEM medium with Danshentong ⅡA in for1hour, and simulate ischemia then reperfusion with DMEM. The activation of Notch signaling pathway and level of HIF-la mRNA was detected by real-time PCR. Production of MDA in myocardiocytes was tested by colorable reaction. Cell apoptosis was observed through AnnexinⅤ-PI staining.Results:In the SI/R group, Notch pathway related signals, Notch and Hesl mRNA level was upregulated. Intra-cellular MDA level and HIF-1mRNA were increased, considering oxidative stress induced after ischemic/reperfusion injury. Ischemic/reperfusion injury also leads to the risen of cell apoptosis and cell death. DAPT is a Notch pathway inhibitor, it prevents SI/R induced oxidative stress, cell apoptosis and cell death. Chinese medicine monomer Danshentong IIA appears to have the same action such as DAPT.Conclusions:Chinese medicine monomer DanshentongⅡA may protect cardiomyocytes from ischemic/reperfusion injury through inactivate Notch pathway and inhibite Notch-related intra-cellular oxidative stress. |
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