目的 通过建立大鼠心肌缺血模型与人脐静脉内皮细胞（HUVECs）缺氧模型，探究当归补血汤（DBD）通过调控自噬促进缺血心肌血管新生的作用机制。方法 SD雄性大鼠随机分为6组：假手术组、模型组、麝香保心丸（SBP，阳性对照，20 mg·kg^-1）组和DBD低、中、高剂量（1.56、3.12、6.24 g·kg^-1）组，除对照组外，采用冠状动脉左前降支结扎术制备大鼠心肌缺血模型，术后2 d开始ig给药，每天1次，给药7 d； 2,3,5-氯化三苯基四氮唑（TTC）染色观察大鼠心肌梗死面积；苏木精-伊红（HE）染色法观察心肌组织病理损伤变化；酶联免疫吸附法（ELISA）检测血清中血管内皮生长因子（VEGF）及碱性成纤维细胞生长因子（bFGF）的表达水平；透射电镜观察心肌超微结构及自噬小体的产生； Western blotting测定心肌组织中自噬相关蛋白Beclin-1、自噬微管相关蛋白轻链3（LC3）-Ⅱ/I的表达；免疫荧光共定位法观察自噬相关蛋白LC3与血管因子CD31的阳性共表达情况。体外培养人脐静脉内皮（HUVECs）细胞，分为6组：对照组、单给DBD（400 mg·L^-1）组、单给DBD（400 mg·L^-1）＋3-MA（5 mmol·L^-1）组（常氧条件下培养）以及模型组、DBD组、DBD＋3-MA组（缺氧培养24 h）。通过CCK-8法检测细胞存活率； Transwell实验评估细胞迁移能力； Matrigel实验检测细胞管腔形成能力； Western blotting检测细胞中自噬相关蛋白Beclin-1、LC3-Ⅱ/Ⅰ的表达。结果 体内实验结果显示，与模型组比较，DBD可显著缩小大鼠心肌梗死面积（P＜0.01），改善心肌组织病理损伤，显著上调血清中VEGF及bFGF的表达水平（P＜0.01）；明显改善心肌组织中线粒体受损程度、减轻空泡化，且自噬小体数量增多，心肌组织中自噬相关蛋白LC3-Ⅱ/Ⅰ、Beclin-1表达水平显著上调（P＜0.01），LC3与CD31免疫荧光阳性共表达率显著提高（P＜0.01）。体外实验结果表明，与模型组相比，DBD可显著提高缺氧条件下HUVECs活力、促进细胞迁移及管腔形成，并上调自噬相关蛋白LC3-Ⅱ/Ⅰ、Beclin-1的表达（P＜0.01）；加入自噬途径抑制剂3-MA后，DBD的上述作用被抑制（P＜0.01）。结论 DBD可促进大鼠缺血心肌血管新生，其作用机制可能与调节自噬反应有关。

Objective To explore the mechanism of Danggui Buxue Decoction (DBD) promoting angiogenesis in ischemic myocardium through regulating autophagy by establishing a rat model of myocardial ischemia and a hypoxia model of human umbilical vein endothelial cells (HUVECs). Methods SD male rats were randomly divided into six groups: sham operation group, model group, Shexiang Baoxin Pills (SBP, positive control, 20 mg·kg^-1) group, and DBD low, medium, and high dose (1.56, 3.12, and 6.24 g·kg^-1) groups. Except for the control group, myocardial ischemia models were established in rats by ligation of the left anterior descending coronary artery. Drug administration via ig route began two days after surgery, once daily for seven days. The rat model of myocardial ischemia was prepared by ligating the left anterior descending coronary artery. The myocardial infarct size in rats was observed by 2,3,5-triphenyltetrazolium chloride (TTC) staining. The pathological damage of myocardial tissue was observed by hematoxylin-eosin (HE) staining. The expression levels of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in serum were detected by enzyme-linked immunosorbent assay (ELISA). The ultrastructure of myocardium and the generation of autophagosomes were observed by transmission electron microscopy. The expression of autophagy-related proteins Beclin-1 and LC3- II/I in myocardial tissue was determined by Western blotting. The co-expression of autophagy-related protein LC3 and vascular factor CD31 was observed by immunofluorescence co-localization. Human umbilical vein endothelial cells (HUVECs) were cultured in vitro and divided into six groups: control group, DBD (400 mg·L^-1) group, DBD (400 mg·L^-1) + 3-MA (5 mmol·L^-1) group (cultured under normoxic conditions), and model group, DBD group, DBD + 3-MA group (cultured under hypoxic conditions for 24 h). Cell viability was detected by CCK-8 assay. Cell migration ability was evaluated by Transwell assay. Cell tube formation ability was detected by Matrigel assay. The expression of autophagy-related proteins Beclin-1 and LC3-Ⅱ/Ⅰ in cells was detected by Western blotting. Results In vivo experimental results showed that DBD could significantly reduce the myocardial infarct size in rats (P < 0.01), improve the pathological damage of myocardial tissue, and significantly up-regulate the expression levels of VEGF and bFGF in serum (P < 0.01). It could significantly improve the damage degree of mitochondria in myocardial tissue, reduce vacuolization, increase the number of autophagosomes, significantly up-regulate the expression levels of autophagy-related proteins LC3-II/I and Beclin-1 in myocardial tissue (P < 0.01), and significantly increase the co-expression rate of LC3 and CD31 immunofluorescence (P < 0.01). In vitro experimental results showed that compared with the normal control group, the viability of HUVECs was significantly decreased after 24 h of hypoxia treatment (P < 0.01). DBD could significantly improve the viability of HUVECs under hypoxic conditions, promote cell migration and tube formation, and up-regulate the expression of autophagy-related proteins LC3-II/I and Beclin-1 (P < 0.01). After adding the autophagy pathway inhibitor 3-MA, the above effects of DBD were inhibited. Conclusion DBD can promote angiogenesis in rats' ischemic myocardium, and its mechanism may be related to the regulation of autophagic response.

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国家自然科学基金青年基金项目（81303262）；山西省应用基础研究计划项目（202303021211176）；山西省重点研发计划项目（201903D321211）；山西省中医药管理局科研课题（2022ZYYC104）；黄芪资源产业化及产业国际化协同创新中心建设经费(XN2026052_090)；山西中医药大学研究生实践创新项目(X2026SJ032)