摘 要：本研究旨在探讨银杏（Ginkgo biloba L.）叶提取物（GBE）对脑梗死（CI）Sprague-Dawley大鼠（Rattus norvegicus）的治疗作用及其潜在机制。通过颈外动脉注射荧光微球诱导动脉多发性阻塞的发生，从而构建CI大鼠模型。将造模成功的大鼠随机分为CI组、丁苯酞（NBP）组、GBE低剂量（GBE-L）组、GBE高剂量（GBE-H）组和GBE-H+沉默调节蛋白7（SIRT7）抑制剂97491（SIRT7i）组，每组20只。另选20只健康大鼠作为对照（Control）组。治疗结束后，对各组大鼠进行神经功能缺损评分；2，3，5-三苯基氯化四氮唑（TTC）染色检测大鼠CI面积；苏木精-伊红（HE）染色观察大鼠脑组织病理变化；酶联免疫吸附试验（ELISA）试剂盒检测脑组织中血管内皮生长因子（VEGF）、血管生成素（Ang）和血小板衍生生长因子（PDGF）水平；免疫荧光检测大鼠脑缺血皮层区白细胞分化抗原31（CD31）阳性表达；蛋白免疫印迹（WB）法检测脑组织中SIRT7/血管内皮生长因子A（VEGFA）通路相关蛋白表达水平。结果显示：与Control组相比，CI组大鼠脑组织病理损伤加重，神经功能缺损评分明显升高（P<0.05），CI面积明显增加（P<0.05），VEGF、Ang、PDGF水平，CD31阳性表达以及SIRT7、VEGFA、VEGF2R蛋白表达水平明显降低（P<0.05）；与CI组相比，NBP组、GBE-L组和GBE-H组大鼠脑组织病理损伤有明显改善，神经功能缺损评分明显降低（P<0.05），CI面积明显减少（P<0.05），VEGF、Ang、PDGF水平，CD31阳性表达以及SIRT7、VEGFA、VEGF2R蛋白表达水平明显升高（P<0.05），其中GBE-H组效果最好。SIRT7i部分逆转了GBE对CI大鼠血管生成的促进作用（P<0.05）。因此，GBE能够改善大鼠CI后血管生成相关反应，减轻脑组织损伤。这可能与SIRT7/VEGFA信号通路的激活有关。
关键词：银杏叶提取物；脑梗死；沉默调节蛋白7/血管内皮生长因子A信号通路；血管生成；神经功能
中图分类号：R743；R285.5     文献标志码：A     DOI：10.3969/j.issn.1007-7146.2026.04.011

Abstract: This study aims to investigate the therapeutic effects of Ginkgo biloba extract (GBE) on Sprague-Dawley rats (Rattus norvegicus) with cerebral infarction (CI) and its potential mechanisms. A CI rat model of multiple arterial occlusion was established by injecting fluorescent micropheres via the external carotid artery. The rats with successful model induction were randomly divided into a CI group, a butylphthalide (NBP) group, a low-dose Ginkgo biloba extract (GBE-L) group, a high-dose Ginkgo biloba extract (GBE-H) group, and a GBE-H plus sirtuin 7 (SIRT7) inhibitor 97491 (SIRT7i) group, with 20 rats in each group. An additional 20 healthy rats were selected as the Control group. Following treatment, neurological impairment scores were assessed across all rat groups. 2, 3, 5-triphenyltetrazolium chloride (TTC) staining was employed to quantify cerebral infarct volume. Haematoxylin and eosin (HE) staining was used to examine pathological changes in brain tissue. Enzyme-linked immunosorbent assay (ELISA) kits were utilized to measure levels of vascular endothelial growth factor (VEGF), angiopoietin (Ang), and platelet-derived growth factor (PDGF) in brain tissue. Immunofluorescence was used to detect cluster of differentiation 31 (CD31) positive expression in the cortical area of rat cerebral ischemia. Western blot (WB) analysis was used to measure the expression levels of proteins associated with the SIRT7/vascular endothelial growth factor A (VEGFA) pathway in brain tissue. The results showed that, compared with the Control group, rats in the CI group exhibited worsened pathological damage in brain tissue, significantly increased neurological impairment scores and cerebral infarct area (P<0.05), and markedly reduced levels of VEGF, Ang, PDGF, CD31-positive expression, as well as SIRT7, VEGFA, and VEGF2R protein expression level (P<0.05). Compared with the CI group, the NBP, GBE-L, and GBE-H groups exhibited significantly improved pathological damage in rat brain tissue, markedly reduced neurological impairment scores, and decreased cerebral infarct area (P<0.05). Levels of VEGF, Ang, PDGF, CD31-positive expression, SIRT7, VEGFA, and VEGF2R protein expression level were markedly elevated (P<0.05), with the GBE-H group demonstrating the most pronounced effects. SIRT7i partially reversed the pro-angiogenic effects of GBE in CI rats (P<0.05). Therefore, GBE can improve angiogenesis-related responses after CI in rats and alleviate brain tissue damage, which may be related to the activation of the SIRT7/VEGFA signaling pathway.
Keywords: Ginkgo biloba extract; cerebral infarction; sirtuin 7/vascular endothelial growth factor A signaling pathway; angiogenesis; neurological function
（Acta Laser Biology Sinica, 2026, 35(4): 376-384）