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银杏叶提取物对缺氧性视网膜神经节细胞变性的神经保护作用及 。

Neuroprotective Effect of Ginkgo Biloba Extract Against Hypoxic Retinal Ganglion Cell Degeneration and .

机构信息

1Department of Ophthalmology, Gyeongsang National University Changwon Hospital, Gyeongsang National University, School of Medicine, Changwon, Korea.

2Department of Ophthalmology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.

出版信息

J Med Food. 2019 Aug;22(8):771-778. doi: 10.1089/jmf.2018.4350. Epub 2019 Jul 3.

Abstract

Hypoxia-induced oxidative stress and disturbed microvascular circulation are both associated with pathogenesis of glaucoma. Ginkgo biloba extract (GBE) has been reported to have positive pharmacological effects on oxidative stress and impaired vascular circulation. This study aimed to investigate the neuroprotective effect of GBE against hypoxic injury to retinal ganglion cells (RGCs) both and . The rat RGC line was used, and oxidative stress was induced by hydrogen peroxide (HO) . EGb 761, a standardized GBE, or vehicle was applied to RGCs. Hypoxic optic nerve injury was induced by clamping the optic nerve of rats with a "microserrefine clip" with an applicator, which was applied without crushing the optic nerve. This method is different from "optic nerve crush model" and does not involve elevation of intraocular pressure, and may serve as a possible normal tension glaucoma animal model. EGb 761 at various concentrations or vehicle was administered intraperitoneally. RGC density was measured to estimate the survival both and . The survival of RGCs was significantly ( < .001) higher upon treatment with 1 or 5 g/mL of EGb 761 compared with vehicle after oxidative stress RGC density upon treatment with EGb 761 of 100 mg/kg (1465.6 ± 175 cells/mm) or 250 mg/kg (1307.6 ± 213 cells/mm) was significantly higher ( < .01,  < .05, respectively) than that obtained with vehicle (876.3 ± 136 cells/mm) . Our results suggest that GBE has neuroprotective effect on RGCs against hypoxic injury both and .

摘要

缺氧诱导的氧化应激和微血管循环障碍均与青光眼的发病机制有关。银杏叶提取物(GBE)已被报道对氧化应激和血管循环受损具有积极的药理作用。本研究旨在探讨银杏叶提取物(GBE)对体外过氧化氢(HO)诱导的视网膜神经节细胞(RGC)氧化应激损伤的保护作用,同时建立大鼠视神经夹伤模型,观察 GBE 对正常眼压性视神经损伤的保护作用。采用大鼠 RGC 细胞系,用 H2O2 诱导氧化应激,用 EGb761(一种标准化的 GBE)或载体处理 RGC。用带有给药器的“微结扎夹”夹闭大鼠视神经来诱导缺氧性视神经损伤,这种方法不同于“视神经钳夹模型”,不涉及眼压升高,可能作为一种正常眼压性青光眼的动物模型。用不同浓度的 EGb761 或载体经腹腔给药。通过测量 RGC 密度来评估两种情况下的存活情况。与载体处理相比,氧化应激后用 1 或 5μg/ml 的 EGb761 处理时,RGC 密度显著升高(<0.001)。用 100mg/kg(1465.6±175 个细胞/mm)或 250mg/kg(1307.6±213 个细胞/mm)的 EGb761 处理时,RGC 密度显著高于载体处理组(<0.01,<0.05)。这些结果表明,GBE 对体外过氧化氢诱导的 RGC 氧化应激损伤和正常眼压性视神经损伤均具有神经保护作用。

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