目的 探究银杏内酯B（ginkgolide B， GB）是否通过拮抗内质网应激（endoplasmic reticulum stress， ERS）发挥其拮抗血管内皮损伤作用及其相关分子机制。 方法 建立衣霉素（tunicamycin， TM）诱导的人骨髓来源内皮祖细胞（bone marrow derived-endothelial progenitor cells， EPCs）ERS损伤模型，用MTS检测细胞增殖能力；Calcein-AM/EthD-I双染法检测细胞活性状态；Transwell实验检测细胞迁移能力；DCFH-DA染色检测活性氧（reactive oxygen species，ROS）的水平；ELISA法测定NADPH活性；JC-1和DiOC6染色定性和定量检测线粒体膜电位；qRT?PCR检测mRNA的水平；Western Blot检测蛋白表达水平。 结果 GB浓度依赖性减轻衣霉素对hEPCs造成的ERS内皮损伤（细胞活性、细胞迁移率和血管形成率的降低）（P < 0.01）；降低ROS及NADPH水平（P < 0.01）；呈浓度依赖性抑制ERS介导的线粒体膜电位下降（P < 0.01）；抑制ERS相关蛋白（GRP78、ATF4、CHOP等）表达，并调控细胞凋亡相关蛋白（Bcl-xl、Bax、cleaved caspase-4、cytochrome c）的表达水平，拮抗内质网应激介导的细胞损伤。 结论 银杏内酯B能通过拮抗内质网应激，发挥血管内皮保护作用，其机制可能与降低细胞内活性氧水平，抑制ERS相关蛋白（CHOP， GRP78、ATF4）表达及调节细胞凋亡蛋白（Bcl-xl、Bax、cleaved caspase-4、cytochrome c）的表达水平有关。

Objective To investigate the potential of ginkgolide B （GB） in mitigating vascular endothelial injury by antagonizing endoplasmic reticulum stress （ERS） and elucidate its underlying molecular mechanism. Methods An injury model of human bone marrow?derived endothelial progenitor cells （EPCs） induced by tunicamycin （TM） was established. Cell proliferation was assessed using MTS assay， while cell viability was determined through Calcein?AM/EthD?I double staining. Transwell assay was employed to evaluate cell migration ability. DCFH?DA staining was utilized to measure intracellular ROS levels， and NADPH activity was quantified via ELISA. JC?1 and DiOC6 staining were performed for qualitative and quantitative assessment of mitochondrial membrane potential respectively. Qrt?pcr analysis was conducted to determine mRNA expression levels， whereas western blot analysis enabled detection of protein expression levels in the cells. Results GB dose?dependently attenuated tunicamycin?induced ERS?mediated endothelial injury in hEPCs， as evidenced by decreased cell viability， impaired cell migration， and angiogenesis inhibition （P < 0.01）. Furthermore， GB treatment significantly reduced ROS production and NADPH levels within the cells （P < 0.01）， while also inhibiting ERS?mediated decline in mitochondrial membrane potential concentration?dependently （P < 0.01）. Additionally， GB inhibited the expression of ERS?related proteins such as GRP78， ATF4， CHOP etc.， regulated apoptosis?related protein Bcl?xl， Bax cleaved caspase?4 cytochrome c； thereby effectively counteracting endoplasmic reticulum stress?induced cellular damage. Conclusions GB exerts a protective effect on vascular endothelium by antagonizing endoplasmic reticulum stress； this mechanism may be attributed to its ability to reduce intracellular reactive oxygen species levels. It also suppresses the expression of ERS?related proteins （CHOP78 and ATF4），and modulates apoptosis?associated proteins （Bcl?xl， Bax， cleaved caspase?4， and cytochrome c）.