中国神经再生研究(英文版) ›› 2022, Vol. 17 ›› Issue (6): 1267-1268.doi: 10.4103/1673-5374.327344

• 观点:周围神经损伤修复保护与再生 • 上一篇    下一篇

啤酒花提取物保护视网膜神经节细胞作为青光眼的新型神经保护策略

  

  • 出版日期:2022-06-15 发布日期:2021-12-17

Retinal ganglion cell protection by hop-flower extract as a novel neuroprotective strategy for glaucoma

Tomoko Hasegawa, Hanako Ohashi Ikeda*   

  1. Department of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan (Hasegawa T, Ikeda HO) Research Fellow of Japan Society for the Promotion of Science, Tokyo, Japan (Hasegawa T)
  • Online:2022-06-15 Published:2021-12-17
  • Contact: Hanako Ohashi Ikeda, MD, PhD, hanakoi@kuhp.kyoto-u.ac.jp.
  • Supported by:
    The present study was supported in part by research grants from the Ministry of Health, Labour and Welfare of Japan (to HOI).

摘要: Neural Regen Res:啤酒花提取物预防视网膜神经节细胞死亡
     前期研究表明谷氨酸-天冬氨酸转运蛋白 (GLAST) 敲除小鼠表现出慢性视网膜神经节细胞死亡和视神经变性而没有升高的眼压,被用作具有正常眼压的青光眼模型。与 GLAST (+/-) 小鼠相比,GLAST (-/-) 小鼠的视网膜神经节细胞受损更严重。使用光谱域光学相干断层扫描检查视网膜厚度,由视网膜神经纤维层、视网膜神经节细胞层和内丛状层组成的神经节细胞复合体在接受啤酒花提取物治疗的 8 周龄和 12 周龄 GLAST (-/-) 小鼠中比未接受治疗的小鼠更厚。外层视网膜的厚度,由外核层、光感受器肌样区、光感受器椭球区和外段层组成,在接受啤酒花提取物治疗的小鼠和未治疗的小鼠之间无显著差异。在接受啤酒花提取物治疗后 12 个月大 GLAST (+/-) 小鼠中,视网膜神经节细胞数量高于未治疗小鼠。接受啤酒花提取物的 18 个月大 GLAST (+/-) 小鼠的视神经比未处理小鼠的视神经更粗。啤酒花提取物减轻了青光眼小鼠模型中视网膜神经节细胞的死亡。 
     来自日本京都大学的Hanako Ohashi Ikeda团队认为,降低眼压是唯一确定的青光眼治疗方法。在某些情况下,尽管眼压充分降低,但视野丧失仍在继续。可能与青光眼有关的一个因素是复发阿尔茨海默病,这是由大脑中Aβ的积累引起的。Aβ在患有高眼压症的青光眼动物模型中的积累。Aβ诱导凋亡性视网膜神经节细胞死亡。考虑到 Aβ 诱导视网膜神经节细胞死亡,减少Aβ积累并因此防止视网膜神经节细胞死亡可能是青光眼的治疗策略。在青光眼小鼠模型中,啤酒花提取物可有效对抗视网膜神经节细胞死亡。这可能为青光眼提供一种潜在的新型治疗策略。
     文章在《中国神经再生研究(英文版)》杂志2022年 6  月  6 期发表。
https://orcid.org/0000-0001-9572-8659 (Hanako Ohashi Ikeda) 

Abstract: In glaucoma, a leading cause of blindness, retinal ganglion cells are progressively damaged. Intraocular pressure reduction is the only established treatment for glaucoma (Collaborative Normal-Tension Glaucoma Study Group, 1998; Vass et al., 2007). However, in some cases, visual field loss progresses despite sufficiently reduced intraocular pressure (Collaborative Normal-Tension Glaucoma Study Group, 1998; Killer and Pircher, 2018). While intraocular pressure and age are known risk factors for glaucoma (Ernest et al., 2013), the underlying mechanisms of glaucoma progression are not fully understood. Many factors that may influence glaucoma progression, including myopia and blood flow impairment, have been investigated (Marcus et al., 2011; Ernest et al., 2013). A factor that may be related to glaucoma is the concurrent occurrence of Alzheimer’s disease, which is caused by the accumulation of amyloid β (Aβ) in the brain. Glaucomatous retinal changes in patients with Alzheimer’s disease have been reported (Wang and Mao, 2021). Other studies have reported Aβ accumulation in animal models of glaucoma with ocular hypertension (Guo et al., 2007; Ito et al., 2012). Moreover, Aβ induces apoptotic retinal ganglion cell death (Guo et al., 2007). Considering that Aβ induces retinal ganglion cell death, reducing Aβ accumulation and consequently preventing retinal ganglion cell death may be a therapeutic strategy for glaucoma (Figure 1A).