Palmhof Marina, Wagner Natalie, Nagel Clarissa, Biert Nora, Stute Gesa, Dick H Burkhard, Joachim Stephanie C
Experimental Eye Research, University Eye Hospital, Ruhr-University Bochum, In der Schornau 23-25, 44892, Bochum, Germany.
Experimental Eye Research, University Eye Hospital, Ruhr-University Bochum, In der Schornau 23-25, 44892, Bochum, Germany.
Exp Eye Res. 2020 Sep;198:108133. doi: 10.1016/j.exer.2020.108133. Epub 2020 Jul 6.
Retinal ischemia leads to an early severe damage of the retina and thus plays an important role in eye diseases such as angle-closure glaucoma or retinal vascular occlusion. In retinal diseases, there is common sense about the affection of the optic nerve by ischemic injury. However, the exact dynamic processes of this optic nerve degeneration are mainly unclear. In this study, retinal ischemia was induced in one eye of Brown-Norway rats by raising the intraocular pressure 60 min to 140 mmHg followed by natural reperfusion. Optic nerves were analyzed at six different points in time: 2, 6, 12, and 24 h as well as 3 and 7 days after ischemic injury. Cell infiltration and moreover signs of tissue demyelination and dissolution were noticed in optic nerves 7 days after ischemia (hematoxylin & eosin: p < 0.001, luxol fast blue: p = 0.04). Although microglial activation was verified already from 12 h on after ischemia (p = 0.030), the beginning of a structural degeneration of the neurofilament was seen at 3 days (p = 0.02). Interestingly, proliferative microglia were present later on (7 days: p = 0.017). At this point, the number of total microglia was also increased in ischemic nerves (p = 0.003). Concluding, our data indicate that not only retinal tissue is affected by an ischemia, the optic nerve also demonstrates progressive damage. Interestingly, a microglia activation was noted days before structural damage became visible.
视网膜缺血会导致视网膜早期严重受损，因此在诸如闭角型青光眼或视网膜血管阻塞等眼部疾病中起重要作用。在视网膜疾病中，缺血性损伤对视神经的影响已为人所熟知。然而，这种视神经变性的确切动态过程主要尚不清楚。在本研究中，通过将棕色挪威大鼠的一只眼眼压升高至140 mmHg并持续60分钟，随后自然再灌注，诱导视网膜缺血。在缺血损伤后的六个不同时间点对视神经进行分析：缺血后2、6、12和24小时以及3天和7天。缺血7天后在视神经中观察到细胞浸润以及组织脱髓鞘和溶解的迹象（苏木精和伊红染色：p < 0.001，卢戈氏碘液快速蓝染色：p = 0.04）。尽管缺血后12小时就已证实小胶质细胞激活（p = 0.030），但在3天时可见神经丝结构变性的开始（p = 0.02）。有趣的是，增殖性小胶质细胞随后出现（7天：p = 0.017）。此时，缺血神经中小胶质细胞总数也增加（p = 0.003）。总之，我们的数据表明，不仅视网膜组织会受到缺血影响，视神经也会出现进行性损伤。有趣的是，在结构损伤可见之前数天就注意到了小胶质细胞激活。
