| Objective：This study established myocardial ischemia-reperfusion model, usingsulforaphane activate the Nrf2-ARE signaling pathway was observed Nrf2-AREsignaling pathway in mouse myocardial ischemia-reperfusion injury in myocardialprotection and related mechanism.Methods:1This experiment uses clean grade, male, sexual maturity, C57black mice45inthe left anterior descending coronary artery ligation manufacturing myocardialischemia-reperfusion injury model (30minutes ischemia).2The mice were randomly divided into three groups: simple myocardial ischemia-reperfusion injury group (model group), myocardial ischemia-reperfusion injury+sulforaphane(Nrf2activator, SFN) intervention group (intervention group) sham group(control group); each group was postoperative1,3,5d at three time points were dividedinto three subgroups (n=5).3Sulforaphane intervention group was given by intraperitoneal administration of1mg/kg, after1times/d; model group and sham operation group were injected withnormal saline, after1times/d.4In each group at corresponding time points (postoperative1d,3d,5d) removethe heart, the required cardiac tissue by HE staining and pathological changes ofmyocardial tissue immunofluorescence Nrf2/HO-1double-labeled positive cells.5The data were statistically analyzed to observe the Nrf2-ARE signaling pathwayon myocardial ischemia-reperfusion injury in rats and related mechanism.Results:1）With the model group and the sham group, the intervention group to reduceinflammatory injury (P<0.05);2）The intervention group of Nrf2/HO-1double-labeledpositive cells are more than the model group and the sham operation group (P<0.05). Conclusion:1) The model of myocardial ischemia-reperfusion injury in the presence of acuteinflammatory injury;2) Sulforaphane activated Nrf2-ARE signaling pathway reducesmyocardial ischemia-reperfusion injury model suppress the inflammatory response andimprove antioxidant enzyme HO-1expression improve myocardial protection. |
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