心肌梗死（MI）是全球备受关注的问题，死亡率高达50%。心肌细胞是终末细胞，目前治疗方法不能修复或逆转己坏死的心肌。文献报道，骨髓间充质干细胞(BMSCs)移植治疗 MI 能促进心功能恢复，但植入心肌后易受大量自由基的损害。氧化应激是导致体内自由基产生和缺血性心肌损伤的主要因素，而Nrf2-ARE是体内尤为重要的抗氧化应激通路。本课题组研究发现，中药降香中新黄酮latifolin对心肌缺血损伤具有显著保护作用，其机制与调控NrF2/ARE通路抗氧化应激有关；同时发现其可以通过激活ERK磷酸化促进BMSCs增殖，表明能增强BMSCs活性。因此，本课题拟在原有工作基础上，利用现代药理学与分子生物学手段，研究latifolin对氧化应激环境下心肌细胞及BMSCs的影响，并基于NrF2/ARE通路探索三者之间的关联性，阐明latifolin治疗心梗的分子调控机制，为临床治疗缺血性心脏病开辟新途径。

Myocardial infarction（MI） received much attention around the world, with a mortality rate over 50%. Cardiomyocytes are terminally differentiated cells. MI is difficult to regenerate and repair. Nowadays there is no effective treatment to repair or reverse the necrotic myocardium. According to the literatures, BMSCs transplantation therapy for MI could improve cardiac function effectively. However, most MSCs of transplantation could not survive in hypoxia circumstance. Oxidative stress is the main factor that leads to the generation of free radicals and ischemic myocardial injury in vivo.Nrf2-ARE pathway plays a crucial role in anti-oxidative stress. Our previous studies demonstrated that new flavonoids latifoiln in Dalbergia odorifera has cardioprotective effect against myocardial hypoxia injury due to its antioxidant action via regulation the Nrf2-ARE pathway. Our studies also found that latifoiln could promote BMSCs proliferation mediated by ERK phosphorylation. These indicated that latifoiln could increase the activity of BMSCs. Therefore, this topic is based on the original work, we try to use modern pharmacology and molecular biology methods to investigate the effect of latifoiln on myocardial cells and BMSCs in oxidative stress circumstance and explore the relationship among them on the NrF2/ARE pathway. The project will clarify the molecular mechanism of latifolin in the treatment of myocardial infarction and provide a new way for clinical treatment of ischemic heart disease.