Abstract：
This research delves into the effectiveness of Ginkgolide B (GB), a compound from Ginkgo biloba, in combating cell death caused by glaucoma, with a focus on mitochondrial impairment and the mitochondrial permeability transition pore (mPTP). Utilizing models of high intraocular pressure and in vitro glaucoma simulations, the study investigates GB\'s impact on retinal progenitor cells (RPCs) under oxygen-glucose deprivation/reperfusion (OGD/R) and in a rat glaucoma model. The study methodologies included apoptosis assessment, apoptotic marker analysis via Western blot, and mitochondrial structure and function evaluation. The findings reveal that GB notably decreases apoptosis in RPCs exposed to OGD/R in vitro, and reduces ischemia-reperfusion damage in vivo. GB\'s protective role is attributed to its ability to preserve mitochondrial integrity, maintain membrane potential, regulate calcium levels, and inhibit mPTP opening. These results underscore GB\'s potential as a therapeutic agent for acute primary angle-closure glaucoma, highlighting its capability to alleviate mitochondrial damage and apoptosis in RPCs and retinal nerve fiber layer cells.
摘要：
本研究探讨了银杏内酯B(GB)的有效性，一种来自银杏叶的化合物，在对抗青光眼引起的细胞死亡方面，重点研究线粒体损伤和线粒体通透性转换孔(mPTP)。利用高眼压模型和体外青光眼模拟，这项研究调查了在氧糖剥夺/再灌注（OGD/R）和大鼠青光眼模型中GB对视网膜祖细胞（RPCs）的影响。研究方法包括细胞凋亡评估，通过Westernblot进行凋亡标记分析，线粒体结构和功能评估。研究结果表明，GB显著降低体外暴露于OGD/R的RPCs的细胞凋亡，并减少体内缺血再灌注损伤。GB的保护作用归因于其保持线粒体完整性的能力，保持膜电位，调节钙水平，并抑制mPTP打开。这些结果强调了GB作为急性原发性闭角型青光眼治疗剂的潜力，强调其减轻RPCs和视网膜神经纤维层细胞线粒体损伤和凋亡的能力。
