目的 观察银杏叶提取物对急性脑缺血小鼠脑皮质缺血的影响，并探讨其对Toll样受体4（TLR4）/核因子-κB（NF-κB）通路的影响。方法 选取60只成年健康雄性CD1小鼠，随机分为假手术组、模型组、阳性对照（3×10⁴ IU/kg乌司他丁）组及银杏叶提取物低、中、高剂量（10、20、40 mg/kg）组，除假手术组外其余5组均建立急性脑缺血小鼠模型。建模成功后，各组小鼠分别尾iv给予相应药物，假手术组和模型组均给予等量生理盐水。观察小鼠脑皮质病理变化和组织学分级；对比各组存活神经元密度；比色法检测脑皮质组织丙二醛（MDA）水平，黄嘌呤氧化法检测小鼠脑皮质组织超氧化物歧化酶（SOD）水平；实时荧光定量PCR（qRT-PCR）法检测小鼠脑皮质组织Toll样受体4（TLR4）、核转录因子NF-κB p65（NF-κB p65）mRNA表达；Western blotting法检测脑皮质组织TLR4、NF-κB p65蛋白表达。结果 假手术组小鼠脑皮质组织结构正常，细胞饱满且排列紧密、有序；模型组小鼠脑皮质组织结构严重受损，细胞严重皱缩，排列紊乱；乌司他丁组和银杏叶提取物各剂量组小鼠病理变化均减轻，且呈剂量依赖；与假手术组比较，其余5组小鼠组织学分级、脑皮质组织MDA水平均升高（P<0.05）；与模型组比较，乌司他丁组和银杏叶提取物各剂量组小鼠组织学分级、脑皮质组织MDA水平均下降（P<0.05）；与乌司他丁组比较，银杏叶提取物高剂量组小鼠组织学分级、脑皮质组织MDA水平均下降（P<0.05）。与假手术组比较，其余5组小鼠脑皮质存活神经元密度、脑皮质组织SOD水平均下降（P<0.05）；与模型组比较，乌司他丁组和银杏叶提取物各剂量组小鼠存活神经元密度、脑皮质组织SOD水平均升高（P<0.05）；与乌司他丁组比较，银杏叶提取物高剂量组小鼠存活神经元密度、脑皮质组织SOD水平升高（P<0.05）。与假手术组比较，其余5组小鼠脑皮质组织TLR4、NF-κB p65 mRNA及蛋白表达均升高（P<0.05）；与模型组比较，乌司他丁组和银杏叶提取物各剂量组小鼠脑皮质组织TLR4、NF-κB p65 mRNA及蛋白表达均下降（P<0.05）；与乌司他丁组对比，银杏叶提取物高剂量组小鼠脑皮质组织TLR4、NF-κB p65 mRNA及蛋白表达水平均降低（P<0.05）。结论 银杏叶提取物可减轻急性脑缺血小鼠脑皮质缺血所致的病理改变，减轻神经功能受损，改善脑皮质组织氧化应激指标，推测其可能是通过调控TLR4/NF-κB p65信号通路，抑制TLR4、NF-κB p65 mRNA及蛋白表达实现的。

Objective To observe the effect of Ginkgo biloba extract on cerebral cortical ischemia in mice with acute cerebral ischemia and explore its effect on Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) pathway. Methods Sixty adult healthy male CD1 mice were randomly divided into sham operated group, model group, positive control group (3×10⁴ IU/kg ulinastatin) and Ginkgo biloba extract low, medium and high doses (10, 20, 40 mg/kg) groups. The acute cerebral ischemia model in other five groups were all established except sham operated group. After successful modeling, mice in each group were given corresponding drugs iv tail, sham operation group and model group were given the same amount of saline. The pathological changes and histological grades of the cerebral cortex were observed. The survival neuron density of each group was compared. Malondialdehyde (MDA) and superoxide dismutase (SOD) were measured by colorimetry and xanthine oxidation respectively. The expressions of Toll like receptor 4 (TLR4) and nuclear transcription factor NF-κB p65 (NF-κB p65) mRNA were detected by real-time fluorescent quantitative PCR (qRT-PCR). Western blotting was used to detect TLR4 and NF-κB p65 protein expression. Results In sham-operated group, the structure of cerebral cortex was normal, and the cells were full and arranged tightly and orderly. In the blank control group, the structure of cerebral cortex was severely damaged, and the cells were severely shrunk and disordered. Pathological changes in the Ulinastatin group and Ginkgo biloba extract groups were alleviated and dose-dependent. Compared with the sham operation group, the other five groups showed higher histological grade and MDA level in cerebral cortex (P < 0.05). Compared with the model group, the histological grade and MDA level of cerebral cortex decreased in ulinastatin group and Ginkgo biloba extract groups (P < 0.05). Compared with ulinastatin group, the histological grade and MDA content of brain cortex decreased in high dose group (P < 0.05). Compared with the sham operated group, the density of surviving neurons and the level of SOD in the other five groups decreased (P < 0.05). Compared with the model group, the density of survival neurons and the level of SOD in cortex increased in ulinastatin group and Ginkgo biloba extract group (P < 0.05). Compared with ulinastatin group, the density of survival neurons and the level of SOD in cortex increased in high dose group (P < 0.05). Compared with the sham operated group, the expression of TLR4, NF-κB p65 mRNA and protein in the other five groups increased (P < 0.05). Compared with the model group, the expression of TLR4, NF-κB p65 mRNA and protein in cortex of mice in ulinastatin group and Ginkgo biloba extract group decreased (P < 0.05). Compared with ulinastatin group, the expression of TLR4, NF-κB p65 mRNA and protein in the brain cortex of mice decreased in the high dose group (P < 0.05). Conclusion Ginkgo biloba extract can alleviate the pathological changes caused by cerebral ischemia in mice with acute cerebral ischemia, alleviate neurological impairment, and improve oxidative stress indexes of cerebral cortex tissues. It is presumed that it may be achieved by regulating TLR4/NF-κB p65 signaling pathway and inhibiting the expressions of TLR4 and NF-κB p65 proteins.